PB89132203
 CHEMICAL, PHYSICAL, AND BIOLOGICAL
   PROPERTIES OF COMPOUNDS PRES1HT
      AT HAZARDOUS WASTB SIT2S
            Final Report
            Prepared  fort

U.S. Environmental Protection Agency




            Prepared  byi

      Clement Associates, Inc.
        1515 Wilson Boulevard
     Arlington, Virginia  22209


        Under  Subcontract  tot

           GOt Corporation
    Bedford, Massachusetts  01730
         Septeaber 27, 1985
      REPRODUCED BY
      U.S. DEPARTMENT OF COMMERCE
           NATIONAL TECHNICAL
          • IN FORMATION SERVICE
           SPRINGFIELD, VA 22161

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50272-101
  REPORT DOCUMENTATION
         PABE
                         I
i,   REPORT NO.
EPA/530-SW-89-010 '
  3.  Recipient's Accession No.
I  W8  9-132203?*$
  4,   Title and Subtitle
      CHEHICAL PHYSICAL,  AND BlQUJBICAl  PROPERTIES DP COMPOUNDS PRESENT AT
      HAZARDOUS WASTE SITES  (FINAL REPORT)
                                                           5.   Report Dace
                                                           9/27/35   	
  7.  Authorfs)
      CLEMENT ASSOCIATES,  INC.
                                                           i,  Performing Organization Rept.  No
  ?.  Performing Organization  Name and Address

      CLEMENT ASSOCIATES,  INC.
      1515 WILSON BOULEVARD
      ARLINGTON, VA 22209
                                                           10.   Praject/Tisk/Work  Unit  No.
                                                           11.   Cantract(C)  or Grant(QJ  No.
                                                           (CI
                                                           (6)
  12.   Sponsoring Organization  Name and Address
      U.S.  EPA
      OFFICE DF SOLID WASTE
      401 M STREET,  SW
      WASHINGTON, DC 20460	
                                                           13.  Type of Report I Period Covered
                                                           FINAL REPORT - 1985
                                                          _.
  15.  Supplementary Nates
  le.  Abstract (Unit:  200  words;

  Thi chemical profiles  are  intended  to  serve as a concise reference with infonsatim on the ptiysicocheiical properties,
  transport and fate,  toxicity, and regulatory standars for individaul cnemicals identified  by  the Office of Waste
  Prograi Enforcement  (EPA)  at  hazardous waste sites.  These profiles can be used in conjunction  with  the Toxicology and
  Endanqerment Assessment Handbooks.
  17.  Document Analysis   a.   Descriptors
      b.  Identifiers/Open-Ended Terns
      c.   COSfiTI Field/Group
  18.   Availability Statement

    RELEASE UNLIMITED
                                        19.  Security Class (This Report;j  21.   No.  of -Pages
                                         UNCLASSIFIED
                                        20.  Security Class (This Page)
                                         UNCLASSIFIED
                 21.  Price
(See ANSI-Z39.18)
                                                                     OPT ONAL FORfl 272  (4-77S
                                                                     (Formerly NTIS-35)

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                            DISCLAIMER

     These- profile* have not undergone final review within
EPA, and they are for 1PA use and distribution only.  Th«y
should not b* construed to represent EPA policy.

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                           INTRODOCTIOM

     Early in 19S4, Clement Associates was requested under Subcon-
tract No. 1-625-999-222-003 to OCA Corporation to provide support
to the EPA Office of Waste Programs Enforcement  {OWPE)  in prepar-
ing a catalog of chemicals of concern at hazardous waste sites.
Clenent was given primary responsibility for two phases of this
task.  First, Clement was to assist GCA in developing an on-line
catalog of chemicals present at hazardous waste  sites.  Second,
Clement was to prepare profiles summarising the  chemical, physi-
cal, and biological properties of these chemicals.  The chemical
profiles are intended to serve as a concise reference with inf^r-
mation on the physicochemical properties, transport and fate,  tox-
icity, and regulatory standards for individual chemicals identi-
fied by OWPE at haaardous wast* sites.  They are not meant to  be
thorough, quantitative reviews and should not be used as substi-
tutes for a good literature review on the characteristics of the
specific chemicals of concern at a particular sit*.
     During the first pLasc, Clement staff searched the consent
decrees, administrative orders, and complaint files obtained from
OWPB foi^b*} names of toxic chemicals detected at enforcement
sites.  iBtf recorded the chemicals present at eacb site,  the
media in which the chemicals were detected, and  the highest  con-
centration of each chemical in a particular medium.  This  informa-
tion was sent to OCA for inclusion in a computer data  base.  Also
during this phase of the task, Clement developed diehotomous
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scores  for each chemical  indicating, whether or not it had any of
the  following characteristics!  carcinoganicity, reproductive
toslcity/teratogenlclty,  mutagenicity, acute toxicity, chronic
toxicity, toxicity to domestic animals, and toxicity to terres-
trial and aquatic wildlife.  The  liat of chemicals compiled and
the  crittcia used for reaching these dlcbotonous determinations
arc  included in Appendix  A to thia  report.
     During the aeeond phasa, Cleaent prepared profiles on the
toxic chemicala that had  been detected at hazardous waste sites.
These profiles are based  aainly on  secondary sources, but the pri-
mary literature was consulted when  necessary.  Bach chemical pro-
file has five sectlonst   Chemical and Physical Properties, Trans-
port and Fate, Health effects, Toxicity to Wildlife and Domestic
Animals, and Regulations  and Standard*.  A short aummary? an
introduction presenting the CAS registry number, chemical formula,
IUPAC name, synonyms and  trade names of the compound, and back-
ground  information (where needed);  and a reference list were also
included.
     These profiles can be used in  conjunction with the Toxicology
and Bndangerment Assessment Handbooks.  These handbooks present
conceptsflgtf Wiimrmition  that are important in understanding the
health events and other  properties of pollutants identified at
hazardous waste sites.
     Brief descriptions of the various sections'of the profiles
and a general list of references  are presented below.
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                                           available
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Chemical and Physical Properties
     Information on the  following chemical and physical  properties
were obtained for each of the profiled compoundst
     atomic_or Molecular Weightt  The weight of  an  atom  or mole-
cule of a chemical expressed in atomic mass units.   One  atomic
mass unit equals one-twelfth the mass of  a carbon-12 atom.
     Boiling Pointi  The temperature in degrees  Celsius  at which
the vapor pressure of the compound  is equal to or  slightly greater
than the atmospheric pressure  [760  mm of  mercury(Bg)K
     Melting Pointi  The temperature in degrees  Celsius  at which  a
material changes from a  solid state to a  liquid  stats at atmos-
pheric pressure.                                               ;
     Specific Gravity!  The weight  of a given volume of  the  com-
pound at a specified temperature relative to the weight  of  an
equal volume of water at 4 degrees  Celsius.
     Solubility in Wateri  The maximum amount of the chemical that
will totally dissolve in water at a given temperature.
     Solubility In Orqanicai  The ability of the chemical to dis-
solve in specified organic compounds at a given  temperature.
     Log Octanoi/Water Partition Coefficienti  The log of the
ratio of Jtbe imatmfc of the chemical that  will totally dissolve in
             iWliiount  that will dissolve  in water.
           Press) or et  The pressure  (usually expressed in milli-
meters of mercury) exerted by  the vapor phase of the chemical in
equilibrium with the solid or  liquid form at a given temperature.
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     7aoqr Densityi   Th« weight  of  a  given  voluas of th« chemical
relative- to  the weight  of  tb*  saae  volume of  ale.
     Henry's Law Constant!   An eapresslon of  th«  distribution of
the chemical between  air and water  at equilibrium.  Usually
defined  as the ratio  of the  partial pressure  of the coapound in
air aeasured in atmospheres  to the  mole fraction  of the compound
In a water solution.
     pKai  A measure  of the  extent  of dissociation of a material,
which  is defined a* the pi at  which half of the con pound la ion-
ized.  pH is defined  as the  logarithm of the  reciprocal of the con-
centration of hydrogen  Ions  In a solution and ranges frost 0 fat)
the most acidic solution to  14 for  the aost basic.            f
     flash Pointt  The  teaperature  at which a flaasiable liquid or
•olid  gives  off enough  vapor to  allow Ignition of the vapor and
ale mixture.

Transport and fats?
     The transport and  fate  of chemicals In th*> environment
depends  on the properties  of both the chemical and the environmen-
tal medium la which It  occurs.  Because of  to* effects of the lat-
ter, th« txamsport and  fat*  of a compound can only b* discussed in
general.SfcmV'^reiTf speciflc  information on  the characteristics of
the environmental medium In  which It  Is present Is not available.
Therefore, the transport and fats section  In the  profiles only
provides general background  Information and will  not apply In all
cases.  For  a more thorough  treatment of the principles governing
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         rbesf available copy.

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chemical movement and fit* In the environment* one of the
reference* listed at the end of this section should be consulted.
     At any specific hazardous wast* facility* the transport and
fate of chemical contaminants must be assessed or modeled based on
site-specific environmental information.  Such assessment or mod-
eling is often a complex task and requires expertise in a variety
of scientific disciplines, including environmental chemistry and
modeling.

Health Effects
     The adverse health effects of greatest concern are those that
cause death or are  irreversible and seriously impair the normal
                                                               -i
functioning of the  individual.  Cancer  is of concern because if] is
so often fatal and  because of the broad agreement that there is  no
safe dose for many  types of carcinogens.  Mutagenicity, or  genetic
toxiclty* is primarily important because an alteration in the
genes of a cell may be the first step in tumor formation and may
cause reproductive  toxicity or teratogenicity.  Reproductive tox-
icity decreases the individual's ability to produce viable  young*
while teratogenicity leads to the production of malformed off-
spring.  Chronic toiicity Involves effects that develop after
long-tens/exposure  (for several years)  to a chemical.  Acute tox-
              ^mmm^-fc_
ieity re£ir» to the effects that result from very short-term,
usually single dose* exposure to a material.  Subchronic exposure
falls between chronic and acute exposure and usually  Involves
exposure to a toxic agent for weeks or  months.  For chronic* sub-
chronic* or acute toxicity* the effects of greatest concern are
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 those that  cause  ••clout  impairment  and  are  irreversible.   For  a
 detailed de*eription of thea«  toxic  affects/  sea  the  Toxicology
 Handbook or on* of  the general references  listed  at the  end of
 this section.
     For thai purposes of  these profiles. Clement  scientists
 atteapted to identify those  effects  of a particular chemical moat
 likely to cause serious bam to exposed  buaan populations.
 Because the profiles are  primarily intended  for as* by EPA per*
 sonnel dealing with haaardous  waste  sites, the toxic  effects
 conaidared  were those most likely to affect  tbe two potentially
 exposed populations!  on-site  workers and  people  living  near t*e
                                                               •
                                                               «
 site*  For  on-site  workers who are exposed to site contaminant*
 for sbort period*,  tbe effects caused by acute or subchronic
 exposure are moat important.   For populations surrounding  a site
 tbat are exposed  to low level* of contamination for long periods,
 cbronie effect* are tbe greatest concern.

 Toxieity to Wildlife and  Domestic animal*
     Toxic  chemicals are  a major concern a*  environmental  contami-
 nants if tbey cause either a potentially irreversible decline in
one or more) specie* or a  decline la  tbe  aesthetics of an area.
                        affect a specie* by  poisoning It*  members
or by reflfttng their food supply. Poleoning can  occur either by
direct exposure in  a contaminated area or, for predator* or scav-
enger*, by  secondary exposure  via contaminated prey or carrion*
The latter  method of exposure  1* of  major  concern because  many
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persistent chemicals can be biomagnified to toxic  levels.
Furthermore, predators and scavengers near the  top of  the  food
chain are fewer in number than prey species and may also be
less able to adjust to a declining population by increasing
reproductive output.  The classic example of this  type of  effect
is the decline in predatory birds in the United States and
Europe due to the ingestion of prey contaminated with  the  per-
sistent organochlorine pesticides, such as DDT.  In addition
to species at the top of the food chain* endangered or threatened
species are of major concern because even a small  decline  in
the population of a species may be enough to cause its extinction,
Regulations and Standards
     Several federal agencies and at least one private associa-
tion have established recommended or mandatory maximum exposure
levels for toxic chemicals.  The U.S. Environmental Protection
Agency (EPA) haa developed health effects assessments  {HEAs)
for chemicals commonly detected at haxardous waste sites.
These RIAs eontala acceptable daily intake levels  for  subchronic
and chronic exposore to noncarclnogens by either Inhalation
or oral routes of exposure and contain CAG unit risks  for  car-
                        SPA has established the Interim Primary
               Standards, which specify the maximum levels
of various chemicals allowable in water used for public consump-
tion.  EPA has also prepared criteria documents on 129 priority
pollutants, which specify the maximum concentrations of these
chemicals in ambient water at which the water can  be regarded
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 as  acceptable  for  the  protection  of  aquatic organisms  and  human
 health.
     The  Carcinogenesis  Assessment Group (CAG)  at EtA  has  per-
 formed carcinogenic  risk assessments on many  compounds.  The
 •unit risks*  (excess risk of  cancer  associated  with lifetime
 exposure  to  1  mg/kg/day  of the chemical) calculated for  these
 chemicals can  be used  to determine levels of  exposure  that
 are likely to  have a low probability of causing cancer.  A
 list of the  unit risks developed  by  CAG and a brief description
 of  this measure is included in Appendix 8 to  this report.
     Several agencies  have developed allowable  exposure  levels*
 for occupational exposure (40 hours  per. week) to airborne  chemf*
 icals.  The National Institute for Occupational Safety and
 Health (NIOSB) has reviewed the available data  on numerous
 industrial materials and published criteria documents  that
 contain recommended  maximum levels of exposure  to these  materials
 in  the workplace.  The Occupational  Safety and  Health  Adminis-
 tration (081A) has established regulations governing exposure
       *
 to  hazardous materials ia the workplace.  These standards  differ
 from VIOn-recommendations in that they are mandatory.  The
 Amer!casa^oafere1!cre  of Governmental  Industrial  lygienlsts  (ACGIH),
 a nongovernmental  association* has also recommended allowable
 exposure  limits for  workplace chemicalsi many of these recom-
mended limits, or  Threshold Limit Values (TLVs), have  been
 adopted as standards by  OSHA.
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     Th« regulatlona, standards, and  recommended  exposure levels
pertaining to each chemical have b«en included  in the  chemical
profiler.  These regulations ware established using  the best
available scientific information, but they «ay  change  at Improved
data become available.  EPA la currently finalizing  the health
effects assessments, proposing recommended maximum contaminant
levels foe drinking water/ and developing health  advisories
for several of the chemicals presented in thasa profiles.
Therefore/ the valuta presented in  the profiles nay  not reflect
currant aciantific information in every case, although they
will be generally applicable.                                  „
                                                               -*
                                                               I
         Reproduced from
            available copy.

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                            REFERENCES
 BUTLER, 3.C. , ed.   1978.   Principles  of  Ecotoxicologyt   Scope  12.
      John Wiley and Sons,  New York

 CONDENSED CHEMICAL DICTIONARY.  1977. 9th  td.   Hawley,  G.S. ,
      ed.  Van Nostrand Rain hold Co.,  New York

 DOULL,  J., KLACJSSEN, D.C., and AMD OR, M.0«   1980.   Casarett
      and Doull's Toxicology:   The Basic  Scisnce  of Poisons.
      2nd ed.   Macnillan Publishing  Co.*  New York

 GUTHRIE, F.B., and PESKY,  J.J., eds.   1980. Introduction to
      Environmental Toxicology.  Blsevier/North Holland,  New
      York

 KHAN, M.A.Q., and BEDERKA, J.P., Jr., eds.   1974.   Survival
      in Toxic Environments.  Acadeaic Presc, N*tf York

 TEE MERCK INDEX.  1976.  9th  «d. Wlndholi, M.,  «d.  Merck
      and Co., Rahway, New  Jersey                              :

 MOORE,  3.W. ,  and MOORE, B.A.   1976.  Enviroraiental Chemistry.
      Acadeaic Press, Hew York

 ODDM, E.P.  1971.   Pundaaentals of  Ecology, 3rd ed.  W.B. Satin-
      ders, Philadelphia

 PATTY* 3 INDUSTRIAL HYGIENE AND TOXICOLOGY.   1978.   Vol.  Is
      General  Principles.   3rd ed.   Clayton* G.D.,  and Clayton,
      F.B., eds.  Wiley-Inter science,  New York

 SAX, N.I.  197S.  Dangerous Properties of Industrial  Material*.
      4th ed.   Van Host rand Reinhold Co., Hew York

 SOFTET, l.i.   1977.  Fate  of  Pollutants  in the Air and Water
      Environaents.  Wiley- Inter science,  Mew York

 THIBODBAUX, L.J.  1979. Cheaodynaaicsi   Bnvironaental Movement
                    n Air,  Water, and  Soil.   Wiley-Inter science,
 TIMBRBLL^  J.A.   1982.   principles of Biocheaical Toxicology.
     Taylor  and Francis Ltd.,  London

 TINS LEY, i.J.   1979.   Chemical Concepts in Pollutant Behavior
     Wiley-Inter science, New York

 0.S. INVIRONHEHTAI, PROTICTIOW AG1NCY (USEFA) .  1979.  Water-
     Related Environaental Fate of 129 Priority Pollutants.
     Washington, D.C.   December 1979.  SPA 440/4-79-029
Preceding page blank
                           M

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VBRSCHUEJUni, K.
     Cbaaicals.
                 1977.  Handbook of Bnviroru««ntal  Data  on  Organic
                 Van Hostrand Reinhold Co., Raw fork.   659 pages
NBAST* BvK
             ad.  1981.  Handbook of Chaaistry and  Physics,
               CRC Prass, Cleveland, Ohio.  2,332 p«f««
                                                                    J

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                    CHEMICAL PROFILES

Ch«»tc«I                               CAS Kuatxr
Ac«naphth«n«                             83-32-9
Ac«naphthyl«n«                          208-96-8
Aettle acid                              €4-19-7
Actton*                                  67-14-1
Acrol«In                                107-02-8
Acrylonitril*                           107-13-1
Aldrin/DUldrlit                         309-00-2
                                         «0-S7-1
Mnio («) aatbrtctn*
                                        120-12-7
                                       7440-36-0
                                       7440-31-2
                                       1332-21-4
                                       7440-39-3
                                         71-43-2
                                         I2-I7-S
                                         56-55-3
                                         95-16-9
                                       7440-41-7
Butanol                                  71-36-3
CadaiOB                                7440-43-9
Carbon t«trachlorid»                    56-23-5
Cblordan*                                S7-74-9
 Reproduced from
 . best available copg..
                       13

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Chlorin*
Cblojrobaiisaaa
Cblorobanzilata
Chloroathana
bi»(2-Chloro«thoxy)«thana
bi«(2-Cbloro«thyl}«th«r
Cblorofora
p-Chloro-B-eraaol
l-Cbloro-3-ni tr ob«n»ana
CbroaiuM
Cobalt
Copptf
Crtsoli
Cyanide
Cymnurie acid
DOT
DlbfOBOClllorOfffOfMIHI
 *       or o«t h«n«
    •*= ,».
1 / 2-Dlcblor o« th«n«
1 i 1-Dichloroa thyl«n«
2 f 4-Dicbloroph«nol
2»4>0ieblocoph«noxyac«tio acid
CAS Kuab+r
7782-50-5
 510-15-6
  7S-00-3
 112-25-5
 111-44-4
  67-6S-3
  Sf-SO-7
 121-73-3
7440-47-3
 211-01-9
7440-41-4
7440-50-8
1311-77-3
  S7-12-S
 108-80-5
  50-29-3
  9C-12-I

  75-34-3
 107-06-2
  75-35-4
 15«-«0-5
 120-19-2
  §4-71-7
   R*produecd from
   best available copy.
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   Ch««ical        -                      CAS
   l,2-Wchlocopropan«                     78-87-5
   l,3-Diehloroprop«n«                    542-75-6
   Dicofol                                115-32-2
   DUthyl phthaltt*                       84-66-2
   Dliiobutyl kcton*                      108-83-8
   DiB«thylMino«thyl m«thacryl«t«       2439-35-2
   Dim«thyLtnilln«                        121-19-7
   DiJt«thylnitro«aain«                     62-75-9
   2 , 4-Diwthylph«nol                     105-67-9
   n-Dioctyl phth*l*t«                    117-84-0
   l,4-9ioxan«                            123-91-1
   Diph«nyl«th«n«                        1103-29-7
   End r In                                  72-20-8
   Zthanol                                 64-17-5
   Zth*nol«jiin«                           141-43-5
   Ethyl actta**                          141-78-6
   Ethylb«nj«n«                           100-41-4
   Bthyl«n«/dt«thyl«n« glycol             107-21-1
                                         111-21C-6
   BtHfl *fctec                              60-29-7
      a..?s
   BtMtteittiVrol                         94-96-2
      w
   biafj-tthylh«xyl)phth*lat«              117-81-7
   Fluotaath«nt                            206-44-0
   Formal d«hyd«                             50-00-0
   H.ptachlot                               76-44-8
Reproduced 
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                                       C*S Ituabag
 Haxachlorob«niana
 Baxaehlorobutadiana
 Haiachlorocyclohaxana
 Kaxaehloroathana
 Haxachlorophana
 Haxana
 Iron
 Iiobutyl  alcohol
 Ifopropyl at bar
Lithi
Manganaa*
Maccury
Mathacrylic acid
Mtthanol
Mtthyl chlorida
Mathylan* eblorlda
       «thyl  katona
       iaobatyl katona
Matbyr parathlon
Bapb thai ana
Hickal
Hitrocallaloaa
Witrophanol
     Reproduced from
     besl available
 Hi-74-1
  87-SS-3
 CO 8-73-1
  67-72-1
  70-30-4
 110-54-3
7439-89-6
  78-83-1
 108-20-3
7439-92-1
7439-93-2
7439-93-4
7439-96-5
7439-97-6
  79-41-4
  67-36-1
  74-87-3
  7S-M-2
  7S-§3-3
 108-10-1
 298-00-0
  91-20-3
7440-02*0
9004-70-0
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 Cfnalcai
CAS Numb«r
 P«nt»chloroph«nol                       87-86-3
 fh*nanthr*n*                            85-01-8
 Phtnol                                 108-9S-2
 Ph«nyl *th*f                           101-84-8
 Phosphorio acid                       7664-38-2
 Phoiphorua (whit*)                    7723-14-0
 Picric acid                             88-80-1
 Polychlorinat«d blph*nyl*             1336-36-3
 Polychlorlnatad dib«nao-p-dloxin»
 Polycyclic aromatic hydrocarbon*
 S«l«nium                              7782-40-2
 Sllv*r                                7440-22-4
 Sodium                                7440-23-3
 Sodium chlorat*                       7775-09-9
 Stoddard golv«nt                      80S2-41-3
 1,2,4,5-T*tfmchlorob«ni«n«              §5-04-3
 2,3,7,8-Tatrachloro-                  1746-01-6
   d1b*nso-f-diosla
 l,l,2,2-T«trachloro«than«               79-34-5
 T*U»ciiloro*thyl*n*                    127-18-4
 Tat^i*ihyTT*ad                         78-00-2
 iMtraBydrofaran                        100-00-0
 Thallium                              7440-28-0
 Titanium                              7440-32-6
 Tolu«n«                                108-88-3
Reproduced from
best available

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Ch«aieal                   '           CAS
                                      8001-35-2
Trichlotob«n*«n«»
2,3,6-Trlchlorob«nzoic acid             50-31-7
l,l,l-Trichloro«th*n*                   71-55-5
l,l,2-Trichloro«th»n«                   7 9-0 a- 5
TrlelUoro«tliyl«ii«                       79-Ol-f
Trichlorofluoro««th«n«                  75-69-4
2,4,5-Trichlocoph«nol                   95-95-4
2,4,S-Trlchloroph«noxyac*tlc acid       93-71-5
2,4,5-Trichloroph«no»y propionic acid   93-72-1
tri«(2,3-Dibrcmopropyl)pho«ph«t«       126-72-7
Vantdiua                              7440-62-2
Vinyl chlorld*                          75-01-4
Xyltnc*                               13 30-20-7
Sine                                  7440-«6-«
                          1%                                    J

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                           ACEXAPSTSXHS
     Acenaphthene .is a  two-tinted polycyclic  aromatic hydrocarbon
 (PAH)_.  Although little specific information  on  acenaphthene
 it available,  information on  related  PAHs  suggests  that  acenaph-
 thene.-is not "yery persistent  in the environment  and that biodegra-
 dation it the  ultimate  fata process.  Acenaphthene  baa not
 been shown to  be carcinogenic or mutagenic, but  it  does  cause
 liver and kidney damage at high exposure
CAS Numben  13-32-9

Chemical Formulat  ci2Hlo

IUPAC Samei  Acenaphthene                                        |


Chemical and Phvaical Prooertie-a

Molecular Weigbtt  154.21

Boiling Point»  279*C

Melting Points  9f.2*C

Specifie Gravityt  1.225 at  0*€

Solubility in If a ten  3.42 mg/liter  at 2S*C

Solubility in Organicai  Soluble  in  ethanol,  toluene,  chloroform,
                                 r  and  acetic  acid
Log OctinayraterPartitiop Co«fficienti   4.33

Vapor Pre«Kret  Leaa  thaa  0.02  msi Hg at  20*C
          ''*S

Vapor Densityt  5,32


Transport and fate

     Acenaphthene,  like  other  polycyclic  aromatic hydrocarbons
(PABs)t can .be emitted into the  environment by both natural and
Acenaphthene
Page 1              1 Rtproduced from
October 1985

-------
 anthropogenic sources.   Sine* very little information in avail-
 Able on this compound specif ically, its environmental fate
 it largely inferred from data for PAfls in general.   fa air,
 acenaphthene can be transported as adsorbed setter  on suspended
 particulates.  Ambient air samples- eollacttd in Sydney, Australia,
 contained a. 07 tig/ 100 m, indicating that atmoapberic transport
 occur a and tbat individuals in uzban environments may b« exposed
 to measureable levels*
      Xa surface watar,  dlract,  rapid pbotolvala of diaaolvad
 acanapbthana .»ay ba an  important vater-ralated anvironaantal
 fata.  It  ia  probabla that ainflat o«yfaa ia the oxidant and
 that  the reaction products are  quinonea.   Volatilisation may
 play  a rola in acenaphtbena transport,  depending on mixing
 rates In both the water and air columns.   However, adsorption
 to sediments  is probably the dominant Sfuatie transport proceaa.
 Consideration of the log ootanol/vatar  partition coaffielant
 for acanapb thane and of the behavior of other PABs indicates
 that  acenaph thane eaa ba strongly adsorbed onto suspended and
 •edimentary particulate matter, especially partieulataa high
 in organic content.
                                                                t
      Based on information concerning related compounds, 1%     |
 is likely  that bioaccumulation  of acenaph thane is short term,  i
 especially for vartebratas.  Although it  is rapidly accumulated?
 after exposure, it also is rapidly metabolised sad excreted.
 Consequently,  bioaccumulation is not considered aa important
 fata  proceaa.   Biodegradation is conaidarad the ultimata fata
 process for acanaphthane.  Baaed oa information foe related
 compounds «  it is probable that  acanapb thane is readily degraded
 by microbes.   Biodegradatioa is likely  to ba> more rapid ia
 the soil than in aquatic systems.  However, studies indicate
 that  biodagradation may ba more important in those) aquatic
 systems that  are chronically affected by  PAH contamination.


 acalth if facts

      •agative reaolta are reported for  a  taat of acenaphthene
 carcinogaoicity besad. upon naoplaatic induction ia the newt
  rltarna agiatstam. bat the reliability of the test ayatam
                aisanlliii carcinogaoiclty  i* not establiahed.
Other eawAofairfvttf studies involving axpoaura to acanapb thane
 as  one; oesHiMnt of eomples mixturea of PAls and other substancaa
 report bow positive sad negative raaulta.  However, the relative
 importsae* off individual component a ia  the mixtures tasted
cannot be  determined, and no conclusions  involving acenaphthene
can ba drawn.   Studies  using several different bacterial test
 systems provide no evidence of  mutagenicity.  Bo information
concerning  its taratoganicity or reproductive toxicity Is avail-
able.
Acenaphthene
Page a
October IttS
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     The most  thoroughly investigated effect of  acenaphthene
 is  iti ability to produce nuclear and cytologieal changes  in
 a variety of aierobial and plant species.  Host  of  these changes,
 •uch as lacreaaes in cell size and DNA content,  art associated
 with a dl»ruption of the spindle mechanism during aitosis  and
 th« resulting  induction of polyploidy.  However, there  is  no
 known correlation between these effects and the  biological
 impact of acenaphthene on mammalian cells.

     Very little is known about the hiaan toxieity  of acenaph-
 thene.  It has been shown to be irritating to the akin  and
 aucous membranes and to cause vomiting if swallowed in  large
 quantities.

     In both rats and mice, subchronic oral exposure causes
 loss of body weight* changes in peripheral blood, increased
 aminotransferase levels in blood serum, and aild morphological
 damage to the  liver and kidneys.  The oral LD10  is  10 g/kg
 for rats and 2.1 g/kg foe aice.  Kidney and liver damage is
 greater after  subchronic exposure to acenaphthene than  after
 acute exposure.


 Toxieity to Wildlife and Domestic JUiiaals
                                                               4
     In acute  toxieity tests for freshwater organisms,  1C..    I
 values of 41,200 and 1,700 ug/litsr are reported for the cxado*
 ceran Daphnia aagna and the bluegill, respectively. In saltwater
 species, 96-hour LC.0 concentration* foe the ayaid  shriap  and   •
 the sheepshead ainno* are 970 and 2,230 pg/liter, respectively.
 A chronic value of 710 ug/liter is reported for  the sheepshead
 ainnow, and the acute-chronic ratio for this species is 3.1.
 No  other aquatic life chronic data are available.   The  freshwater
 alga Selenastrua capricornutua and the saltwater alga Skeletoneaa
 eoatatunare both relatively sensitive to acenaphthene  exposure,
 with 96-hour BC,0 values for chlorophyll a and cell number
 of  approximately"523 ug/liter and 500 ug/liter*  respectively.

     The steady state bioconcentration factor for acenaphthene
 in  the bluegill is 391, vita a tissue half-life  of  less than
 1 day.  By mini the bluegill data and an adjustment factor
 to  allow for> differences la lipid content, the bioconcentration
factor £pf acenaphthene and  the edible portions of  all freshwater
and estfcjiaeuaajatic organisas consumed  by Xaericans is  esti-*
aated Kb* 242.  Reports of acenaphthene in  foods  is limited.
One staeV reports levels of  3*2  uf/kg  (the  detection limit)
or greater in the tissues of shellfish of an unspecified species
and location.

     * study summarising the toxieity  of a  variety of compounds
to wild and doaestic bird species  indicates that the Lb.0 of
acenaphthene for the redwinged blackbird is greater thafTlOO ag/kg,


Acenaphthene
Page 3
October 1985
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-------
 Purthera»re, the study raporta that acenaphthene did not aig—
 nificantly deter feeding by the blackbird even whan It was prt»-
 •iit in foot at relatively high concentrations.

           jt •»

 Regulation* and Standards

 Aabient Hater Quality Critacia (USEPA) t

      Aquatic Lift

      The available data ara inadaquata for aatabliahing final
      criteria.  EPA did report the lowest valves known to causa
      toaicity in aquatic organiama,

      Freshwater

           Acute toxicity*  1,700 pg/liter
           Chronic toiicityi   Ho available data

      Saltwater

           Acute toiicityt  970 ng/liter
           Chronic toiicityi   710 vig/liter                       :
                                                                 •^
      Huaan Health                                               !

    ^  Tha available data ara inadequate for aatabliabing -a human
      health criterion.
                *

      Organolaptic criterion!   20 uf/llta*
SAX, H.I.   197S.  Dangerous Properties of Industrial Materiala.
     4th fed.  van HOBtrand Reinhold  Co.,  Hew York.   1,258 pages

         l.W., lOHLU, W.A.,  and H0RLBOT, J.  1983.   The acuta
     oral toxicity, repellency,  and  haiard potential of 99S
     cbealcala to oo« or »ore  apaciea of wild and domestic
     bird&^Arco. toviron. Contaa.  Toiicol.   12:335-382

U.S. ••i&lllllTll Pliilli Illlll  MIMH I  (USXPA).  1979.  Water-Related
     lavflpflM&fcal Fate  el 139 Priority Pollutants.   Vol. 2.
     Maaaiogton,  O.C.  Dacaabar  1979.  tPA-440/4-7>-0296
                                   Reproduced from
                                   ben available <=opy,
Page 4
October 1985
                                                                     J

-------
0,3. ENVIRONMENTAL PROTECTION AGENCY  (OSEPA).  1980.  Ambient
     Water Quality Criteria for Acenaphthene.  office of Water
     Regulations and Standards, Criteria and standards Division,
     Washington, D.C.  October 1980.  SPA 440/5-80-015

WEAST, R.I., ed.  1981.  Handbook of Chemistry and Physics.
     62nd »d.  CHC frees, Cleveland, Ohio.  2,332 pages
Acenaphthene
tag* 5
October 1985

-------

-------
       Acewaphthylane i« en
-------
data  for tea* PAH§ suggest that oxidation by chlorine or ozone
may be a significant fata process whan thasa oxidants art avail-
•bit  In sufficient quantities.  Volatilisation may play a rola
in acenaphthylene transport dapandinf on mixing ratas in both
tht water column and air eel inn.  For aeanaphthylene, it is
probable* feast adsorption gtnarally_is tht most important aquatic
transport process.  Considtration of ita 109 oetanol/vatar
partition coefficient and of tha behavior of othtr PAHa indicatt
that  actnaphthylana can ba strongly adaorbad onto auspandad
and sedimentary partieulata matter, aspaeially partieulatas
hig>  in organic content.  It ia likaly that this compound can
ba raadily tranaportad as adaorbad matter or suapandtd particu-
latas in air or water*

      Baaad on information concerning ralattd compounds, it ia
likaly that bioaccumulation of acanaphthylana ia short tern,
especially for vertebrataa.  Although PAHa ara rapidly accumu-
lated, they alao ara rapidly metabolized and excreted, and
consequently bioaceuaulation is not eonsidarad an important
fata  process.  PAHS can ba metabolized by multicellular organisms
and degraded by microbaa.  Degradation by mammala is likaly to
ba incomplete, with parent compound and tha metabolites being
excreted by tha urinary ayatem.  Biodegradation by microorgan-
isms  is probably tha ultimata fata proceaa for acenaphthylene.;
Biodegradation generally appaara to ba nor* efficient in soil !
than  in aquatic systems.  However/ experimental data indicate*
that  biodegradation may ba more important ia those aquatic    *
systems that ara chronically affected by PAHs contamination.

     Ataoapheric transport of PAHs can occur* and thasa materiala
can ba returned to aquatic and terrestrial ayatama by wat and
dry deposition.  Some PASS can satar surface aad frouadwatars
by leaching from polluted soils.


Health Effects

     There ara no epid*aiological or case stadias suggesting
that acenaphthylene is carcinogenic in humans.  There ara no
reports of carcinogenic, teratogenic, or reproductive affects
ia experimental aaimala.  Acenaphthylene ia reported to have
weak mutaoaaie activity ia * Salmonella tvphimoriua test system
(Kadaa
            >rmation concerning acuta or chronic tosieity is
            Like many other PAHa, acenaphthylane asy be s skin
irritant, but little spaeifie information is available.
Acaaaphthylaaa
Page 2   -
October IftS
                                                                   J

-------
                              ACETIC ACID
        Acetic acid is • relatively weak acid with a pKa  of  4.7.
   It i* soluble in water.  Acetic acid irritates the skin,  eyes,
   and mucous membrane*, and it may have adverse reproductive
   effects at high dose levels.  Acetic acid vapors are  known
   to form explosive mixtures and toxic fumes when combined  with
   air.


   CAS Number:  64-15-17

   Chemical Formulai  CBjCOOH

   IUPAC Names  Acetie acid

   Important Synonyms and Trade Namesi   Glacial acetic acid, vinegar
                                        acid, ethylic acid,  ethanoic
                                        acidf and methanecarboxylic
                                        acid


   Chemical and Physical Properties              _                 *

   Molecular Weights  60.05

   Boiling Pointt  118»C

   Melting Pointi  li.S*C

   Specific Gravityi  1.05 at 20*C

   Solubility la We ten  Very soluble

   Solubility in Organicsi  Soluble in alcohol, acetone,  benzene,
                            glycerin, ether, and carbon tatrsenioride

   Vapor treasurei  11.4 mm Bg at 20*C

   vapor Density!  2.07

   flasb Polits--  40"C (closed cup)


   Transport and Fate

        •o Information was available on the transport and fate
   of acetic aeid.  However, sosie generalisations can be made
   based on chemical and physical, properties.  Acetic acid is


   Acetic acid
   fage 1
   October ISIS                                     M
Preceding pag^blank

-------
 extremely soluble in water  and therefore is  probably transported
 in surface and  groundwater.   Only a snail amount  it  likely to
 volatilise/ from natural surface water  owing  to its high  solubil-
 ity in water.


 Health Effects

     Acetic acid is  not considered to  be a carcinogen.   Nutagenie
 effects were observed in an assay using  the  aieroorganisa  E«cher-
 iehia  coli. Sex chroaosoae loss and nondiajunction  were reported
 in Prosoph i la aelanogaste_r .   Oral administration  of  700  ag/kg
 to pregnant feaales  produced behavioral  effects in newborn
 rats.

     Acute toxleity  depends on the cheaical  foray the free
 acid is aore toxic than the salt.  Irritant  effects  on the
 human  gastrointestinal tract were seen at concentrations as
 low as 1,470 ug/kg after oral adainistratioa.   Inhalation  pro-
 duced  irritant  effects at an exposure  level  of 100 mg/m  admin-
 istered for 1 hour,  while. severe toxic effects were  associated
 with exposure to 500 ag/a  for the saae  period. The irritation
 caused by acetic acid usually affects  the skin, eyes* aucous    »
 aeabranas,  or the exposed teeth.  Irritant effects on huaans    *
 and aniaals do  not appear to be emulative.  The LD.fl in the    I
 rat given neutralised acetic acid orally was 3,310 if/kg,  while*
 the LD.n value  in aice following intravenous adainistration
 was S2i°mg/kg.

     five workers exposed to high concentration*  (1*6-490  ag/a3
 at peak concentrations)  for  7 to 12 years, experienced short-
 tera loss of sensitivity, conjunctivitis, bronchitis, pharyngitis,
 and erosion of  exposed teeth.  Ingestioa of  concentrations
 between O.Olt and 0.25%  (approxiaately 10-160  ag/kg)  had no
 toxic  effects when adainistered to rats  over a 2- to 4-aonth
   Kriod.   When concentrations of 0.5%,  corresponding  to daily
   ses  of about  330 ag/kg, were administered, an iaaediate  and
 progressive decrease in food consuaptiou cad) growth  was  observed.

     Acetic acid vapors  are  known to fora explosive  mixtures
 and tosie fuaas when combined with air.,


                      and Ooaeatie Animals
     Onljlimlted  information  on  the  toiicity  of  acetic  acid
to aquatic organisas  is available.  Acute  exposure  of  bluegills
and goldfish resulted  in  a  96-hour  BC,Q  of 75  at/liter and
100 mg/liter, respectively.  The  LC«03 for  shrimp  ranged  from
100 to 330 ag/liter when  they  were  exposed for a  41-hour period
in aerated water*  The perturbation level  in the  protosea CVorti-
eella caapanulal was  1! as/liter.  In bacteria Ctseudomonas


Acetic acid
Page 2
October 1985
                                                                    J

-------
 putida),  call aultiplieatlon was  inhibited at  2,850 ag/littr,
 while  §0  »g/liter  inhibited multiplication for  the alga*  (Micro-
 evatia aaruqinosa).

     No Information on  the toiicity of acttic acid to  terrestrial
 wildllf*  or domestic aniaals was  found in tha litaratura  reviewed.


 Regulationa and Standard*

 OSHA Standardf  25 »g/m3 TWA

 ACGIH  Thrtihold Limit Valuaat  25 »g/»J THA
                               37 »f/BJ STEL


 REFERENCES     ..

 NATIONAL  INSTITUTE FOR  OCCUPATIONAL SATBTY AKD  HEALTH  (NIOSH).
     1914.  Rtgiatry of Toxic Effacta of Chaaical Subatanca'i.
     Data iaaa.  Waihington, D.C.  July 1984

 PATTY, P.A.* ad.   19(3.  Industrial Hygiana and Toxicology.
     Vol. 2.  2nd  rav.  ad.  Intaracianca Publiabarar Naw  York.  -.
     2,377 pagaa                                                ;

 SAX, N.I., ad.  197S.   Dangaroua  Propartias of  Industrial Mata-
     riala.  4tb ad.  Van loatrand lainbold Co., Haw fork.
     1,258 pagaa

VERSCHUZREN, K.  1977.  Bandbook  of Bnvironjiantal Data on Organic
    " Chamicals.  van Hoatrand lainbold Co., law fork.  €59 pagaa

WEAST, R.E., ad.   1981'.  Handbook of Caaaiitry  and Physic*.
    ' 62nd ad.  CSC fraaa, Clavaland, Ohio.  2332 pagaa
Acatic acid
Paga 3
Octobar 19IS

-------

-------
                              ACETONE
 Summarg
      Alston* is a commonly used solvent, which probably is
 not very persistent in the environment.  It is considered to
 have rather low toxicity, and no chronic health hazarda have
 been associated with exposure to it.  Acetone Is not very toxic
 to aquatic organisms.

 CAS Number!  67-64-1
 Chemical Formula!  CH3-CO-CH3
 I DP AC tlamet  Propanona
 Important Synonyms and Trada Namesi  Dimethyl katona, 2-propanone
 Chemical and Physical Properties
 Molecular Weight:  58.OS
 Boiling Point!  S6.2*C
 Malting Point:  -9S»C
 Spaclfie Gravity:  0.7199 at 20*C
 Solubility in Water!  miscibla
 Solubility in Organics:  Soluble in alcohol, ether, benzene,
                          and chloroform
 Log Octanol/Water Partition Coefficient:  -0.24
 Vapor Pressuret  190 mm if at 20*C
 Vapor Densityi  2*00
          it*  -1**C (closed cup)
           '*       »
 Transport and Fata
      Very limited information on the transport  and  fata of
 acetent was found in the literature reviewed.   Bowaver, ketones
 in genaral ara probably not vary parsiatent.  Acatona  has a
 high vapor pressure and therefore would be arpected to volatilize
 readily, but because of its high watar solubility,  volatilization
 is probably limited.  Once in the atmosphere, it  is apparantly
 Acatona
 f aga 1
 October 1985
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best avaiSabla copy.
Preceding page blank

-------
 oxidised.   Acetone  has  a  low  octanol/water partition  coefficient
 and therefore  is  probably not readily adsorbed.  Biodegradation
 is probably iaportant in  deteraining the  fate of acetone  in  the
 environment became of  its aliphatic nature.  Evidence of this
 is provided by the  biological oxygen demand value* which was
 72% of  the  theoretical  value  after  20 days at 20*C.


 lealth  Effects

      Acetone has  not been tested  in a earcinogenicity bioaasay
 but gave negative results in  a skin painting test and was not
 autagenic in the  Aaes assay.   Ho  studies  on aniaals for tera-
 togenicity  or  reproductive toxicity have  been done, but acetone
 was negative in a chicken egg injection study for teratogenicity.

      Acetone is generally regarded  as having low toxicity and
 therefore has  not been  extensively  studied.  Prolonged inhalation
 of high concentrations  aay produce  Irritation of the  respiratory
 tract*  coughing*  headache* drowainess* incoordination* and in
 severe  eases,  coma.

      In animal studies* rats  consuming doses of IS ag/kg/day j
 for 4 aontha showed  reduced food  consumption and growth,  in  <
 behavioral  etudiea*  rats  exposed  to §,000 ppm (14*200 ag/a )  '
 acetone for 4  hours/day*  5 days/week for  2 weeks showed modified
 avoidance and-  escape behavior after one exposure* but no changes
 after subsequent  exposures.  At 11*000 ppm  (37,800 mg/m ),
 altered responses were  noted  throughout the 2-week exposure
 period.  Ho chronic  health haxards  have been associated with
 exposure to acetone.


 Toxieitv to Wildlife and  Pomestic Aniaals

      The toxicity of acetone  to aquatic organisms is  lew.
 The  LC50 value for  sunfish was reported to be 14.2 g/liter*
 and  thi threshold concentration for immobilisation of Daphnia
 aagna was reported  to be  over 9 g/liter  (Nclee *nd wolFTfiTF.

      Wo information  on  the toxicity of acetone to terrestrial
 wildllfiCOK  dQiaj£ic animals  was  found in the literature  reviewed,
        *. - -

 Regulations  and Standards

•IOSS Recommended Standard (air)i  250 ppm  (593 ag/a3) TWA

ACCIH Threshold Limit valaeaj 750  ppm U»7SO mg/a3),TifA
                               1*000 ppm  (2,375 mg/a4) STBL
Acetone
>age 2
October 198S

-------
 REFERENCES

 AMERICAN  IKDUSTHIAL BYGIENE ASSOCIATION  (AIHA).   1980.  Hygienic
      Quid*  Barits:  Acetone

 MCXES, J.I.,  and WOLF, H.W.  1963.  Wat*? Quality Criteria.
      2nd  ad.  California State Water ft*BOure*« Control Board
      Publication 3A

 NATIONAL  INSTITUTE FOB OCCUPATIONAL SAFETY AND HEALTH  (NIOSH).
      1978.  Criteria for a Recomaended standard—Occupational
      Expoaura to Ketonea.  Washington, D.C.  DHEW publication
      No.  (NIOSH} 71-173

 NATIONAL  INSTITUTE POX OCCUPATIONAL SAFETY AND HEALTH  (NIOSH).
      1983.  Refiatry of Toxic Bffacta of Chesieal Subatancaa.
      Data Baa«.  Wmahington, D.C.  January 1984

 U.S.  ENVIRONMENTAL PROTECTION AGENCY (GSEPA}.-  1984.  Baalth
      Effaeta  Aaaaaaaiant for Acatona.  Environmental Criteria
      and  Aaaaaaaent Office, Cincinnati, Ohio.  September 1984.
      ECAO-CIN-H016  (Final Draft)

 VERSC1UEREM,  I.  1977.  Handbook of Environmental Data on Organic
      Chemicala.  Van Noatrand Reinhold Co., New York.  659 page*
                                                                *
 WEAST, R.E.f  ad.  1981.  Handbook of Chemiitry and Phyiica.     !
      62nd ad.  CRC Preaa, Cleveland, Ohio.  2,332 pagea
Acatona
page 3
October 1985

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-------
                               ACROLEIN
   Summary

        Acrolein ia an aldehyde that baa been uaed a* a* aquatic
   herbicide.  It if hydrated and then biodegraded in water  and
   probably ia not very persistent in the environment.  Acrolein
   la mutagenic and nay have toxic raproductiv* affteta.  It ia
   a powerful irritant and can cauaa paraanant lung daaafa vhan
   inhaled.
   CAS Numberi  107-02-8

   Chemical Formula*

   IOPAC naaai  2-Propen»l
CH2CHCBO
   Important Synonyma and Trada Raaaas   Acrylic aldehyde;  allylal-
                                        dehyde, 2-propen-l-one,
                                        prop-2-an-l-al,  acrylaldehyde


   Chemical and Phyaieal Prooertiea

   Molecular Weight*  36.1

   Boiling Pointi   S2.S*C

   Melting Points   -86.9»C

   Specific Seavityi  0.1410 at 20*C

   Solubility in Wateri  200 g/liter

   Solubility in Organicat  Soluble in ethanol, ether,  and acetone

   Log Octanol/Water Partition Coefficienti   -0.090
                                                                  *

   Vapor f r««||»«s  ^||§ pa 8f at 20 *C

   Vapor Denatty*  1.94

   Flaab Pointt  -26.1-C
   Acrolein
   Page 1
   October  1985
Preceding page blank

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Transport  and rate

     •ydration  to beta-bydroxypropionaldehyde, followed by bio-
degradation,. is probably  the most  iaportant aquatic fat* for
acrolein.  The)  bait-life  for these processes is reported to
be  less  thany 4  days.  Although volatilisation can occur* its
relative importance as  an environmental process is not known.
No  information  on the photolysis of acrolein in aquatic systems
is  available » but this  process may proceed slowly in the atmos-
phere.   Some oiidation  of acrolein may occur in aquatic systems
and in* 'the atmosphere.  The relatively high water solubility
and the  low  109 octanol/partition  coefficient of acrolein make
sorption and bioaceumulation unlikely environmental processes.


Health Hfeets

     There is no unequivocal evidence to suggest that aerolein
is  carcinogenic in humans or experimental animals.  There are
no  reports of teratogenicity, but  intravenous administration
during gestation is reported to increase postimplantation mor-
tality.  Acrolein also  produces mutagenie effects in a variety
of  test  systems.

     Most  reports of acrolein toxieity are associated with
inhalation exposure.  Aerolein is  a powerful lachrymogen, and
it  is irritating to the eyes and to the mucous membranes of
the respiratory tract.  Irritant effects are) observed in indi-
viduals  exposed to 2.S  »g/sr or less.  Higher concentration*
can cause  persistent lung damage.  Exposure to approximately
350 mg/m*  is reported* to  be fatal  in humans within 10 minutes.

     Lacrimation and irritation of the eyes and respiratory
tract are  the most commonly observed effects in experimental
animals  exposed to acrolein by inhalation.  This compound also
is  reported  to  produce  severe skim irritation.  The Inhalation
and oral LD.n values ia rats are 300 mg/m4 and 46 mg/kg, res-
pectively. 3M


                           mstic  Anmals
               Information  indicates  that acute  and chronic
toxieitf fJtJrefbwmfcer aquatic  life occurs  at  concentrations
as low a*^af and 21 us/liter * respectively.  Acute toxieity
to saltweteY'aquetic life is reported to occur at concentra-
tions as low as 55 ug/liter.  Toxieity would occur at  lower
concentrations among species more  sensitive than those tested.
Aerolein
Page 2
October 1985

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             and  Standards
 Aablent Water Quality Criteria  (DSEPA) »

      Aauatle Lift

      The  available data are not adequate for establishing criteria.

      Hunan Health

      Griterieni  320 pg/liter

 OSHA  standard i   0.25 «g/»3

 ACGIH Threshold  Liait Values:  0.25 «f/a3 TWA

                               0.8 »9/«3 STZL


 REFERJSHC1S

 AMERICAN  CQNF1REMCI OF GOVERNKENTAL IRDOSTRXAL HYC1EHISTS (ACGIH).
      1980*  Documentation of the Threshold Liait Values. " 4th
      ed.  Cincinnati, Ohio.  488 pages

 I8T1RHATIOHAL ACTNCT FOR RESEARCH OR CANCER  (IARC) .  1979.      .
      IARC Monographs on the Evaluation of Carcinogenic Risk     :
      of Chemicals to Huaans.  Vol. lit  Sosie Monovers, Plastic  I
      and  Synthetic  Ilastcmers, and Acrolein.  World Health
      Organization, Lyon, Franc*.  Pp. 479-495

 RATIONAL  INSTITUTE FOR OCCUPATIONAL SAFZTf AMD HKALTI (HIOSH) .
      1984.  Registry of Toxic iffects of CbeoUcal Substances.
      Data Base.  Washington, B.C.  April 1984

 SAX,  R.x.  1975.  Dangerous Properties of Industrial Materials.
      4th  ed.  van Host rand Reinhold Co., Rev fork.  1,258 pages

 O.S.  ENVIRONMENTAL PROTECTI 0« AGTSCT  (USEPA) .  1979.  Water-
      Related Snvironaental Fate of 129 Priority Pollutants.
     Washington, D.C.  December 1979.  IPA 440/4-79*029

U.S.  EWVIJWtlMZNTAL PROTECTION ACBNC?  (DSZPA) .  1980.  Ambient
     Wate* Quality Criteria for Acrolein.  Office of Water
      Resa&tioasand Standards, Criteria and Standards Division,
     WaMMflton7TT;c.  October 1980.  BPA 440/5-80-017

WZAST, m.i. ed.  1981.  Handbook of Chemistry and Physics.
      62nd ed.  dC Press, Cleveland, Ohio.   2,332 pages
Acrolein
Page 3
October 1985

-------

-------
                          ACRYLOHITRILB
     Acrilonitrila i» «n Important chamical  intarmadiata  uaad
in the pfaatlca industry.  It is fairly soluble  in watar  and
is also quita volatils*  Photooaidation. in tha ataoaphara and
biodagradation aca probably Important fataa  in tha snvironnant.
1ARC. has elassifiad acrylonitrila as a auapaetad human  carcinogan,
It eauaaa lung tiaors in huaans and aniaals  aiposad by  inhalation
and "tumors at' othar aitas in axpariaantal aniaala axposad orally.
Acrylonitrila is mutaganic and taratoganic,  and  it ean  daaaga
tha eantral narvoua ayataa, livar and kidnays.
CAS Nuaiban  107-13-1

Chanical Formulai  CH^CHCH

IUPAC waaat  2-Propananitrila

Important Synonyms and Trada naaass  Vinyl  cyanida, cyanoathylena,
                                     proparanitrila             •


Chemical and Physical Propartias

Molacular Waifbtt  53.Of

Boiling foists  77.S to 77.9*C

Malting Pointj  -B3.SS*C

Specific Gravityt  0.8060 at 20*C

Solubility in ITatan  73,500 mg/litar at  20•€

Solubility in Organicss  Solubla in  alcobol* athar, acatona,  and
                         bansana

Log OctaafJk/Vatar Partition Coafficianti  -0.14
         Ji.    jiMt^wc—
vapor Prat«ra»  10 mm Bg at 20 *C
          v,
vapor Dansity*  1.83

Flash Pointi  0*C
Acrylonitrila
Paga 1
Octobar 19S5
     Preceding page blank

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 Transport  and  Fate

      Direct  photolysis of  acrylonitrile  in aquatic environments
 is  unlikely.   However, it  may  react with some naturally occurring
 aromatic tings in the presence of photosensitliing plant pigments
 or  industrially produced dyes.  Such conditions might occur in
 highly polluted surface waters or at a waste site.  Volatilisa-
 tion is a  major environmental  transport  process for acrylonitrile,
 Acrylonitrile  can be volatilised from aquatic and terrestrial
 systems, and transported in the atmosphere as a vapor or adsorbed
 to  partlculates.  Although, aerylonitile  can return to aquatic
 and terrestrial systems in precipitation, photooxidatlon in the
 troposphere  is a significant environmental fate process.  Hydro-
 lysis and  sorptlon- probably are not important fate processes
 under natural  conditions.

      Bioaecumulation of acrylonitrile is not expected to be
 a significant  process, but the cyanoethylation of proteins
 in  aquatic biota may occur.  Acrylonitrile is biodegraded by
 sewage sludge,  but there may be an insufficient population of
 microorganisms ia the- water column and insufficient contact
 time for biodegradation to be  effective  in surface waters.
 In  terrestrial mammals, acrylonitrile can be metabolized to
 thiocyanate  and eliminated in  the urine.  Considerable species .
 and organ  differences in mammals* ability to detoxify acry-
 lonitrile  have been observed.


 Health Effects

      The International Agency  for Research on Cancer (IARC)
 classifies acrylonitrile as a  suspected  human carcinogen.
 Spidemlologic  studies of persons oceupationally exposed to
 this compound  revealed an  excess of cancer at a number of sites,
 but particularly  in the lung.  In a two-year study with acrylo-
 nitrile incorporated ia the drinking water of rats, increased
 incidences of  subcutaneous tumors in the mammary region, Symbal
 gland  carcinomas, central •nervous system astrocytomas, and
 aquamous cell papillomas of the forestomach were observed ia
 animals receiving doses as low as 33 ppsj (approximately 8.73
»g/*9/day).  Acrylonitrile also appears  to be carcinogenic
 in  experimental animals exposed by inhalationy it produces
 long tusMsfs)  in these animals.  Acrylonitrile is mutagenic in
a varietftof tivt-vystems.  It also produces maternal toxicity
and  teraieganlcity in rats after oral or inhalation exposure,
sad  in  hamsters after infcraperltoneal administration.
                                     *
     Acrylonitrile is readily  absorbed from the respiratory
and gastrointestinal tracts, and through the intact skia.
Several studies report toxic effects of  acrylonitrile due to
occupational and  accidental exposures.   These results must
be  interpreted  with caution, however, because the exposures


Acrylonitrile
fage a
October 1983
                                                                     J

-------
are often feo i combination of substances.  Some of th« subjective
complaints reported act headache, fatigue, vertigo, nausea,
weakness, and insosmia.  The clinical syaptoas observed include
aneaia, jaundice, conjunctivitis, aild liver Injury, abnormal
blood and* arine values, and functional disorders of the cardiovas-
cular, heaopoietic, and central nervous systeas.  Contact aller-
gic dermatitis, toxic epideraal necrosis, disturbed iaaunolofical
reactivity, and sensitisation have also been seen.  Impaired
pulmonary function and mortality have been reported in cases
of acute exposure to very high concentrations of acrylonitrile.

     Acrylonitrile, adainistered by various routes, can cause
edeaa in the body organs of Bice, rats, and guinea pigs, as
well as daaage to the central nervous system, liver, and kidneys.
An oral LD«Q of 12 mg/Xg is reported for rats.  Rats and rabbits
that inhalia 250 ag/a3 {114 ppm) of acrylonitrile for 6 months
exhibited changes in peripheral blood patterns! functional
disorders in the respiratory, cardiovascular, and renal systems;
and neuronal lesions in the central nervous .systea.  Soae of
the sane changes were observed at concentrations of SO mg/a       ,
(23 ppa).  An inhalation !£.- of 500 ppa  (approximately 1,100 ng/n )
for 4 hours is reported formats.


Yoxteity to Wildlife and Domestic Animals                      .

     A 48-hour tclfl of 7,550 nf/liter is reported for th*,fcfresi-
water invertebratl Paphnia magna.  Aaong freshwater fish, 96-hour
LC.Q values are 11,800 )tf/liter for the blue gill, 11,100  yg/littr
for the fathead minnow, and 33,500 ug/litec for the guppy.
A 30-day LC.Q value of 2,500 (if/liter is reported for the fathead
minnow.  Data obtained during this study suggest that acrylonitrile
has a definite chronic or cumulative efleet and that adverse
effects can be expected to occur at concentrations below 2,600 ug/
liter in fish exposed for aore than 30 days.


Regulations and Standards

Ambient Water Quality Criteria  (OSEPA)t

     Aguetic Life

                   data are not adequate for establishing criteria.

           Health

     Estimates of the carcinogenic risks associated with lifetime
     exposure to various concentrations of ecrylonitrrle in
     water arei
Acrylonitrile
Page 3
October 1185

-------
                                    Concentration

      *«  *                           0.58 Mi/liter
      10*1                           0.058 jig/liter
      10"'                           O.QG«
 GAG  Unit  Hi* *  (USEPA):  0.24  (

 MXOSH  Recomaended Standards   4 ppa Ceiling Level

 OSHA Standard;   2 ppit TWA  (canctr hazard )
                 10 ppai  CIS-Bin Calling Laval}


 REFERENCES

 AMERICAN  CONFERENCE OF  GOVERNMENTAL INDUSTRIAL HYGIENISTS  (JCGIB),
     1980.  Docunentation of  tha Threshold tiait Values.   4th
     ad.  Cincinnati, Ohio.   488 pagaa

 INTERNATIONAL AGENCY FOR RESEARCH OH CAMdR  (IARC).  1979.
     XARC Monograph* on tha Evaluation of Carcinogenic Risk
     of Chemical* to luaans.  Vol. 19t  S.oaa Itonoaara, Plaatiea
     and  Synthatie Blaatoaara* and Acrolain.  World laalth   .
     Organiiation, Lyonf France.  Pp. 73-113                  |

 NATIONAL  INSTITtm FOR  OCCUPATIONAL SAFETY AMD HEALTH  (MZOfll).
     1983.  Ragiatry of Toxic Iffacta of Cha»icai Suaatancua.
     Data Ba«a.  Washington,  B.C.  Octobar 1983

 SAX, W.I.  1975.  Oang«rou§ PropartitJ of Industrial Mataritla.
     4th  ad.  Vm Mostiand Rainhold Co., Man York.  1,258  pagaa

 O.S. ENVIRONMENTAL PROTICTI OS AGZNCT  (USSPA) .  1979.  Vatar-
     Ralatad Znvironaantal Fata of 129 Priority Pollutant* .
     waahington, D.C.   Dacaabar 1979.  EPA 440/4-79-029

 O.S. ENVIRONMENTAL PROTECTION AGENCY  (USEPA) .  1980.  AmbUnt
     Watar Quality Criteria lot Acrylonitrila.  Office of  Watar
     Jtagulation* and Standard*, Criteria and Standard* Diviaion,
     Waahington, D.C.   Octobar 1980.  IPX 440/5-80*017

U.S. gjmjCPtgJgAju PROTECTION AGENCY  (DSEPA) .  1985.  Raalth
     Aaiaaiaaiant Document for  Dichlorcaiathana  (Mathylana Chloride)
     Off3ca of Health and Environaantal Aaaaaaaant.  Vaahington*
     D.C.  February 1985.  EPA €00/8-82/Q04F

NEAST, R.Z,, ad.  1981.  Handbook of Che«i»try and Phypica.
     82nd ad.  CRC Praaa« Cleveland, Ohio.  2332 page*
Acrylonitrile
Page 4
Octobar 1985
                                                                   J

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                         ALDRIN/DIELORIS
 Summary

     Aldrhi degrades to dteldrin, which is vtry persistent
 in  the environment.  Both pesticides are eareinof«nic in riti
 and ale* and are teratogenic and reproductive toxicant*.  Aldrin
 and dieldrin cause liver toxieity and central nervous system
 abnormalities following chronic expoaura.  Both are also acutely
 toxic,- with oca], LD.Q valuea of about SO Bf/kf.  Both pesticides
 are very toxic to aquatic organisms and have been associated
 with large-scale kills of terrestrial wildlife in treated areas.
Background Information

     Dieldrin is the 6,7-epoxide of aldrin and is readily ob-
tained froai aldrin under noraal environaental conditions aad
by aetabolisa in aniaals.
CAS nuaban  Aldrini  309-00-2
             Oieldeint  60-57-1
Chemical Formulas
Aldrini  C
Dieldrin i
                  HCl
ItTPAC Haaei  Aldrini  Ir2r3,4,10,10-hexachloro-l,4,4«»5,8,8a-
             bexabydro-1,4iS,8-exo-di«ethanonaphthalene

             Dialdrint  l,2r3,4,10r10-hexacb.loro-6,7-epoxy-
             I,4,4a,3,6,7,8,8a-octahydro-endo,exo-l,4i5,8-di
             methanonapbtbalene
 !he«ieal

Molecular
          roperties
fktt  Aldrini  365
      Dieldrini  381
Melting Points  Aldrini  104*C
                Dieldrint   176*C
Aldrin/Dieldrin
Page 1
October 1985

-------
 Solubility In Watan   Aldrini   20 yg/littr at 25*C
                       Ditldrini  200 ug/littr at 25*C

 Solubility in Organic*s   Solublt in most organic solvents

 Log Octanel/Watsr Partition Cotffieitnts  No  data foundr  probably
                                           graatar than  5  for
                                           both cbamicala

 Vapor 9zsssurai   Aldrini   2.31 m 10~S~ui 89 at 20*C
                  Oisldrinj   2.8 x 10~* mm Eg  at 20*C
 Transport and Fata
      Aldrin •vaporate• rapidly froa aquatic anvironmtnts  and
 also probably  from  soil.   Photolysis probably occurs  in tb*
 ataoiphart  altar  volatilization.   Adsorption,.aspacially  by
 organic matsrials,  is also an important  fata procass  foe  this
 chamieal.   Jtldrin is  bioconcantratad by  aquatic organisms by
 a factor of 10 to  10 .   Biotransformation  by aquatic organisms
 and  biodtgradation  art also important fata  procassas.

      Tht priaary  product  of aldrin dagradation is  its tpoxidt,
 dialdrin.   Photolysis of  aldrin also produeas small amounts
 of photoaldrin, pbo tod i aldrin, and s polyiiarisation product.
 Dialdrin is eonsldarad to ba at laast a* toxic as  aldrin  sad
 is quits ptrsistsnt in tha anvironaant.   Tbaraforaf transfor-
 mation  of aldrin  raprasants only  a changa of stata and not
 datoiification of tha chamieal.

      Dialdrin  is  ona  of tha aost  parsistant of tat eblorinattd
 hydrocarbons.  Volatilisation and possibly  subsaquant photolysis
 to photodisldrin  art  important transport and fatt  proctssas froa
 surfact wsttr  and probably froa soil.  Adsorption  to  stdiatnts,
 atpacially  organic  matarials, and bioaccuaolation  art also
 important in ramoving ditldrin froa vatar.   Biotransformation
 and biodagradation  of ditldrin occur vtry slowly but  aay  ba
 tha final fata procassts  ia sadimant.


Health  gffacts
     Beta Bftiflf'aiii ditldrin  art  carcinogana,  causing  inertasts
in a varisfy; °f tumors  ia rats at  low  but not at  high dosts
and producing a bighar  incidanca of  llvti tumors  in  mica.
Tht rtsson for this rtvarstd dott-caaponaa  rtlstionship is
unclaar.  fftithtr spptsrs to bt autagtnie whan  tastad la s
auabtr of systama.  Aldrin and ditldrin  szt both  tosie  to tha
rtproduetivt systta and ttrstogtnie.   Rtproduetivt tfftets
ineludt dtertastd fartility, inertastd fatal daath,  and affacts
on gastationi whilt ttrstogtnie tfftets  ineludt eltft palata,


Aldrin/Dialdrin
ftgs 2
Oetobtr HIS

-------
webbed foot, and skeletal anomalies.  Chronic effects Attributed
to aldrin and dieldrin include liver toxicity and central nervous
•ysten abnormalities.  Both chemicals are acutely toxic; the
oral LD«n is around SO mg/kg, and tht dermal &D.n ii about
100 mg/lgV                                     50


Toxicity to Wildlife and Domestic Animals

     Aldrin and dieldrin ar* both acutely toxic to freshwater
species at low concentrations.  Tests in fish showed that the
two chemicals had similar toxicities, with I*CSfl values ranging
from 1 to 46 tig/litec foe different species. 'Final acute values
for freshwater species were determined to be 2.5 pg/liter for
dieldrin and 3.0 ug/liter for aldrin.  Saltwater species were
also quite sensitive to aldrin and dieldrin.  The range of LC50
values was similar to that for freshwater species*  2 to 100 pgV
liter for aldrin and 1 to 34 tig/liter for dieldrin.  Th« salt-
water Final Acute Values were 1,3 ug/liter for- aldrin and 0.71 ug/
liter for dieldrin.

     Chronie studies have been conducted on the affects of
dieldrin on freshwater and saltwater species,  for freshwater
organisms, chronic values as low as 0.2 t»g/liter were obtained.  .
The Final Acute Chronic Ratio was determined to INI 3.5, and the  .j
calculated Freshwater Final Chronic Value was 0.29 ug/liter.     ,-
Only one chronic study was dona on saltwater species.  Therefor**
the saltwater Final Chronic Value-of 0.084 uf/litac was deter-
mined by dividing the Final Acute value by toe acute-chronic
ratio.  MO chronic studies were performed on aldrLn* but because
its acute toxicity is comparable to that of dieldrin and because
it is readily converted to dieldrin in animals aad in the environ-
ment, it probably has similar chronic toxicity*

     Both pesticides, and especially dieldrin, have been associ-
ated with large-scale bird and mammal kills in treated areas.
Experimental feeding studies have shown that the chemicals
are quite toxic to terrestrial wildlife and domestic animals
at low levels.


Regulations and1 Standards

Ambient titttf Quality Criteria  (OSEPA)i

              ife

     Freshwater

         Acute toxicity»  Aldrini  3.0 ng/liter
                          Dieldrini  2.S uf/liter
Aldrin/Oieldrin
Fage 3
October 1985
                            til

-------
         Chronic  toxicityr  Aldrint  we availabla data
                            Dialdrint  0.0019 pg/litar
      saltwater
          Acute  toiicityt  Aldrini  1.3 gg/lit«r
                          Dialdrint  0.71
         Chronic  toxiclty:  Xldrint  Ho available data
                            Dieldrini  0.0019 ng/liter

     Hunan Italth

     Eatlaataa of tha carcinogenic rialca aasociatad with lifetime
     axpoaura to  varioua concantrationi in watar aras

                       Aide ill                Dialdrin
     Rlali           Concantration          Concantration

     10"!           0.74 Bf/litae          0.71 Bf/lltae
     10"!           0.074 nf/lltar         0.071 nf/litar
     10"'           0.0074 ng/litae        0.0071 af/litar
CAG Unite Ri«k  (U5IPA) i  Aldrin:   11.4               .
                         Dialdrim  30.4  (»9/kg/day)"i

ACGIH Threshold Liait Value:*  0.2S mg/ml TWA
                               0.7S »9/»J STEX,

OSHA Standard (air)i*  2SO M9/«3 TWA
       K.«.  1970.  Aldrin, Dialdrin, ndria and Telodrin.
     Blaaviar Publiahing Co., Haw ford.  234 pagaa

NATIONAL IHSTITDTB FOR OCCUPATIONAL SAFETY AND HEALTH  (NIOSH) .
     1978.  Spacial Occupational Bazar d Ravi aw for Aldrin/DIel-
     drin.  loekvilla, Maryland.  Sapteabar 1978.  DSDHEW Publi
     cation no. 71-301
NATIONAL Hit 190SLJOR OCCUPATIONAL SAFETY AlfD HEALTH  (NIOSH),
     19MJsr lagiatry of Toiic iffacta of Cnaaical Substance*.
     Data iaaa.  Washington, D.C.  October 1913

U.S. ENVIRONMENTAL PROTECTION AGENCY  (USEPA).  1979.  Water-
     Relattd Environmental Fata of 129 Priority Pollutants
     Washington, D.C.  December 1979.  DA 440/4-79-029


* Applies to both aldrin and dialdrin.


Aldrin/Dieldrin
Faga 4
October 1985


-------
 U.S. ENVIRONMENTAL PROTECTION AGEHCY  (OSEPA).  1980.  Ambient
     Water Quality Criteria for Aldrin/Dieldrin.  office of
     Water Regulations and Standards, Criteria and Standards   .
     Division, Washington, D.C.  October 1980.  EPA 440/5-80-019

 5.5. ENVIRONMENTAL PROTECTION AGENCY  (USEPA).  19IS.  Health
     Assessment Document for Dichloromethane  (Methylene Chloride).
     Office of Health and Environmental Assessment.  Washington,
     D.C.  February 198S.  EPA 600/8-82/004?

 VERSCHUEREN, R.  1977.  Handbook of Environmental Data on Organic
     Chemicals.  Van Hostrand Reinhold Co., New Yorfc.  €59 pages

 WEAST, R.B., ed.  1981.  landboofc of Chemistry and Physics.
     62nd ed.  CRC Press, Cleveland, Ohio.  2332 pages
Aldrin/Dieldrin
Page 5
October 1985

-------

-------
                                 ALKANES
    Summary
         The high molecular weight  aikanes  (C,  and  greater)  are
    major- constituents of petroleum.  Their  transport  and  fate  in
    the environment and  their  toxicity depend on  both  their  chain
    length and branching,  in  general, the high molecular  weight
    aikanes are  rather persistent  in  the  natural  environment and
    biodegradation  is probably an  important  fate  process.  These
    long chain aikanes generally are  not  very toxic, but  they are
    irritants and several may  be neurotoxic.  Concentrations of
    100 tag/liter of pentane, ..hexane,  or heptane were not  toxic  to
    young coho salmon, but they did cause irritation.


    CAS Number:

    Chemical Formula:  Cn


    Chemical and_fhyslcal Properties

    Molecular Weight:  14 x number  of carbons + 2

    Boiling Point:  Increases  with  increasing molecular weight

    Melting Point:  Variable,  depending on whether  .there  is  an
                    even or an odd  number of carbons and  on  branching
                     (-91 to 2Q«C)

    Specific Scavity:  Increases with increasing  molecular weight
                        CO.? to 0.3  at 20«C)

    Solubility in Water:  Essentially insoluble in  water;  solubility
                          decreases with  increasing molecular weight

    Solubility in Organics:  Soluble  in benzene,  carbon tetrachleride,
                             chloroformi  and other  aikanes

    Log Octanol/Wattr Partition Coefficient:  Approximately  0.5
                                              multiplied  by  the nudber
                                              of  carbons  in  the
                                               «-!«•»„•».-| m «S *   .->
                                              and increasing ..c;*
                                              slcwly thereafter (calcu

    Vapor Pressure:  Decreases with increasing  molecular  weight
    Aikanes
    Page  1
    October  1935

Preceding page blank

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Transport  and fata

     Only  Iiaite4  information  on  the  transport and face of
alkanes  with high molecular  weights  (i.e.»"ea  and greater)
was  found  in the literature  reviewed.   However/  soa*
estimates  of likely  transport  and  fate  processes can be deter-
mined  from Information  on  shorter  chain alkanes, th* chemical
and  physical properties of the specific compounds, and son*
liaited  data on biodegradation.

     Alkalies art relatively  nonreactive compounds and therefore
art  probably rather  persistent in  the environment.  Branching
tends  to increase stability  so that  the alkaae degrades even
more slowly.  Th* aDcanes  with the higher  molecular weights
have low vapor pressures and probably* are  not  very volatile.
However, their low solubility  in aqueous media and consequent
high level of activity  may make  them at least  somewhat volatile.
Once in  the atmosphere* and  in the presence  of HO , slow photo-
oxidation  to alkanones  will  occur.  ADcanes  with lore than
six  carbons have fairly high 109 octanol/water partition coeffi-
cients and probably  bind readily to organic  materials in soil
and  sediment.  They  are unlikely to be  very  aotile in the en-
vironment.  The principal  fate of  aDcanes  in aquatic and ter-
restrial environments is probably  biodegradation by soil and
aquatic  microorganisms  (laines and Alexander 1974}.  These
microorganisms can convert the alkanes  to  long-chain carboxylie
acids such as oleic  acid (Merdinger and Merdinger 1970).


Health Effects

     Ho  information  was found  suggesting that  the aDcanes are
likely to  be carcinogenic  or mutagenic,  or to  cause reproductive
toxicity.   n-Hexane  has been associated with polyneuropathy in
chronically exposed  workers  and has induced  peripheral nerve
damage in  animal studies.  However, there  is no  evidence that
l:r.;i; shiir* or brar.shti ilkants hav« this s&se  tlfac^;.   :.-.
tests examining suppression  of the action  potential in nerve
cells, longer chai-n  alkanes  were progressively less active
than shorter chain alkanes (Haydon et »1.  1977).   In LCtOQ
studies on 13 C. to  C,, alkanes injected into  mice, Jeppsson
(1975)  noted that toxicity was generally positively correlated
with the nuaber of carbons up  to C8  (n-octane),  after which
*3»i2iv -jsuaii? declined.   The  tl?2.n*a  irt  iljv- '.rrit2r.tr.
. « * *. «, M» M J| f« W K|M-W AJIfMkMIMMtMt.* A|M ^ ^  -|||-fJK*"^K ** m£  *•*<*  •*•««•*» ^ «• «•• "» •[ ^ - — « .
•»«*.«» »«• S - )« «» * V ^- ^ -^ W «»•«•«• -«^B -•*»«».  «tS 'mm**  W«W  *** «_ •»* * «M «, «. ^W «« M
increases, at least  up  to  C? (the  heaviest alkane tested).


Toxicity to wildlife and Domestic  Animals

     Morrow (1974) reported  that pentane,  hexane, and heptane
at levels  of 190 mg/liter  in aerated seawater  were not letr.al


Alkanes
P«ge 2

aeteb"19"

-------
to young Coho saloon but did cause irritation.  Ho deaths  occurred
in mosquito fish exposed for 96 hours to n-h«ptan« at  a  nominal
concentration of 5,SOQ ng/lifir in aerated, turbid water.
(The actual concfntration of alkane in these experiments may
have b«tn lo%mr because of their insolubility, binding to  particu-
latttft and volatilization).  A 24-hour LDSO valut of 4 of/liter
was reported for goldfish exposed to either n-hexane or  n-heptar.e.
Ho other information on the toxicity of alkanes to wildlife
or domestic animals was found in the literature reviewed.


Regulations and Standards

HIOSS Recommended Standard:  360 mg/m3 TWA

OSHA Standard:  1,450 mg/m3 TWA (octant)

ACGIH Threshold Limit Valuta:  1,450 mg/m3 TWA (octane)
1,450 mg/m; TWA
1,800 Bg/aJ STE
REFERENCES
                                           STSL  (octane)
         CONF2REHCS OF GO^SRHMZSTAL INDUSTRIAL KGIENISTS  (ACG115 .
     1980.  Documentation of the Threshold Limit Values.   4th
     ed.  Cincinnati, Ohio.  438 pages

OGULL, J., KLAASSSK, C.D., and AMDOR, M.O., eda.  1980.  Casarett
     and Ooull's Toxicology:  Tht Basic Science of Poisons.
     Ind^e'd." Jfacminan" Publishing Co., New ¥or*.  778 pages

HAIHES, J.R.^ and ALEXANDER, M.  1974.  Hicrobial degradation*
     of high-molecular weight alkants.  Appl. Microbiol.   23:1084-
     108S
        D.A., HZNDRy, B.M., LEVINSON, S.R., and REQOENA, J.
     1977.  Anesthesia of the n-al'kanes':  A comparative study
     of nerve impulse blockage and the properties of black
     lipid bilayer membranes.  Biochira, Biophys. Acta 470:17-34

JZPPSSON, R,  1975.  farabolic relation between lipophilicity
     and biological activity of aliphatic hydrocarbons, ethers,
     and ke tones after intravenous injections of emulsion for- '
     mulations into mice.  Acta Phantacol. Toxicol. 37:56-64
           .  "— SSL,  ~.~    ir.i  v2Sr!!8L.V?T. ".£.- 1-1Z-  lir.-ii^
     of Chemical Property Estimation Methods;  Environraer.:i_
     Behavior of Organic Compounds.  McGraw-Hill Book Co.,
     New
TH2 MTRCJC ZND2X.  1976.  ith ed.  Windholz," M.-, ed.  Merck
     and Co., Rahway, New Jersey
Alkanes
Page 3
October 1985

-------
MEROINGZS, I.i and MERPINCSS, R.P.  1970.  tJtiii*ation of-  n-alkanes
     by Pallalaria aallulana.  20:651-652

MORROW, J.2.  1974.  £ffacts of crude oil and some of its  compo-
     nents on young Coho and Sockaye salnon.  EPA £10/3-73-013

NATIONAL INSTITUTE FOR OCCUPATIONAL SAFOT AND HEALTH (NIQSH) .
     1977.  Criteria for i Recomraended Standard--Occupational
     Exposurt to AlJcants (C5-C-3) ,  Washington, D.C.  DHEW
     Publication No. {NIOSH) 77-1S1

NATIONAL INSTITUTE FOR OCCUPATIONAL SAFSTt AND HEALTH (NIOSH1,
     1984.  Ragistry of Toxic sfftcts of Cntmleal Substances.
     Data Base.  Washington, D.C*  October 1934

SAX, N.I.  1975.  Dangerous Properties of Industrial Materials.
     4th ed.  Van Nostrand Reinhold Co., Nev York.  1,253  pages

VERSCHUZR£N, K.  1977.  Handbook  of Snvironaental Data on  Organic
     Chemicals.  Van Nostrand Reinhold Co.., New York.  659 pages

     / U.S., ed.  1981.  Handbook of Chemistry and Physics.
     62nd ed.  C3C Press, Cleveland, Ohio.  2,332 pages
Alkanes
Page 4
October 1985
                                                                  j

-------
     AlXyl benzenes are a class of compounds that have a single
aromatic ring with one or more aliphatic chains attached.
They art not very persistent in the environment.  Alkyl benzenes
art not very toxic, but at high doses they art irritants and
can cause central nervous system anomalies.  They are generally
toxic to fish at concentrations greater than 4 mg/liter.


Introduction

     Several individual alkyl benzenes, specifically toluene,
xylent, and ethylbenzene, are discussed in separate profiles.
Because the information on other alkyl benzenes ia rather limited
and these compounds are likely to behave rather similarly,
they are considered together in a general profile.  Information
on specific chemicals is provided in the attached table,

Chemical Formula:  C^R (CH)X


Cheaical and Physical Progtrties

Boiling Point:  Directly related to, numbe_r of carbons—1QQ-19Q*C

Melting Point:  Variable, generally around 25*C

Specific Gravity:  Approximately 0.9 at 20*C

Solubility in Waters  Inversely related to number of carbons:
                      Cg—approximately ISO mg/liter
                      c|—approximately 70 mg/littr
                      C^g—approximately IS as/liter

Solubility in Organics:  Soluble in acetone* benzene/ and ether

Log Octanol/Water Partition Coefficient:  Directly related
                                          to number of carbons.
                                          Ct—approximately 3
                                                  rcsiitatelv 3.S
Vapor Pressure: _ Inversely related to number of carbons.
                 Cg—approximately 8 an ig
                 Cj—approximately 3 ma Sg
                 Ct n—approximately 1 mm ig
Alkyl benzenes
Page 1
October 1985

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Transport and Fatt

     Alkyl benzenes will volatilise into the ataosphere  from
both the foil and surface water.  Once in the air,  they  art
a-ttacked &y hydroxyl radicals to fora aldehydes, hydrooxalkyl-
benzenes, and nitroalkylbenzenes; -they art also oxidized,  and
the eh iff product is peroxyacetylnitratt (FAN)'.  The  alkyi
btnztrsts have log octanol/wattr partition coefficients of  3
to 4 and therefore art- probably adsorbed by organics  in  soil
and sediments.  They art also biodegraded by soil and aquatic
microorganisms.  Alkyl btnztnas probably art not vary persistent
In the tnviroruatnt.


Health Effects

     Tht information on the potential health effects  associated
with exposure to the alkyl benzenes with S or more  carbons
is extremely limited.  No data were available on the  carcino-
genic! ty of the alkyl benzenes.  Tht results of mutagtnicity
assays on both ethylbenzene and xylent vert negative.  Ithyl-
benzene and xylene, and presumably the larger alkyl benzenes,
are not teratogtnic, but they do rttard growth somewhat.   The
priaary tffects associated with exposure to the alkyl benzenes
are narcosis, central nervous system anomalies, and irritation,
particularly of the mucous membranes." Oral L0.fl values  in the
rat for the larger alkyl benzenes arts  ethyltfliuene—5,000 mg/fcg;
isopropyl benzene*-!,400 ag/kgr trioethylbenzene--5,OQO  mg/kg;
diethylbenzene—5,000 mg/kg; and tetraae.hylbenzene—6,000 mg/kg.


Toxicity to wildlife and Poiacstic Aniaals

     Very limited information was available on the  toxicity
of alkyl benzenes to wildlife, and none was  'ound en  their
tsxieity to d-wssstlc .aniaals.  In. fish, ff-haur LC5*  values
were generally in the range of 10 to 100 tig/liter.-yInvertebrate
species were apparently afftcttd at similar concentrations.
However, sensitive species were stressed at concentrations
as low aa 4 mg/liter, and young fry were often adversely affected
at still lower concentrations.  These studies vert  conducted
on toluene, ethylbenzene, and xylene, and not on the  longer
chain 
-------
Regulations and Standards

OSHA Standard (skin):  245 mg/m3 TWA (isopropyl benzene)
               *
ACGIH Thteshold Limit- Valuta (skin) ?

     Isopropyl benzenes  245 «g/m; TWA
                         3SS mg/mj STSL

     Trimethyl benzene:  125 ag/m* TWA
                         170 mg/m4 STEL


REFERENCES

AMERICAN CONFERENCE OF GOVERNMENTAL INDUSTRIAL HYGISNISTS  (ACGX3S .
     1180.  Documentation of th* Thctshold Limit Valuei.   4feJi
     «d,  Cincinnati, Ohio.  438 pag«s

DOULL, J,, KLAASSZN, C.D. , and AHD01f H.O., tds.  1980.  Casarett
     and Doull's Toxicology:  The Basic Scitnct of Poisons.
     2nd *d.  Macaillan Publishing Co., New York.  778 pages

LYHAN, W.J., VSttL, W.F., and 10SESBLATT, D.H.  1582.  Handbook
     of Chemical Property Estimation Methods:  Environmental
     Behavior of Organic Compounds.  McGraw-Hill Book Co.,
     New
THE MERCK INDEX.' 1971.  9th ed.  windholz, M., ed.  Merck
     and Co., Rahway, New Jersey

NATIONAL WSTITTJTE WR OCCUPATIONAL SAFETY AND HEALTH  (NIOSH5 .
     1984.  Registry of Toxic Effects of Chemical Substances.
     Data Bast.  Washington/ D.C.  October 1984

NATIONAL RESEARCH COUNCIL (tfRC) .  1981.  The Alkyl Benzenes.
     Committee on Alkyl Benzene Derivatives, Assembly of Life
     Sciences, NRC.  National Academy Press, Washington, :.;.

SAX, N.I.  1975.  Dangerous Properties of Industrial Materials.
     4th ed.  van Nostrand Reinhold Co., Nev York.  1,253 pages

U.S. ENVIRONMENTAL PROTECTION AGENCY*  (OSEPA} .  1979.  Water-  '
    'Related Environmental Fate of 129 Priority Pollutants.
     "«si.-.«-.sa. :..:.  :4-;aasar 1?"?,  iSi  I.4C '4-"*-i:<:? "

WEAST, R.E., ed.  1981.  Handbook of Chemistry and Physics.
     62nd ed.  CRC Press, Cleveland, Ohio.  2,332 pages
Alkyl benzenes
Page 3
October 198S

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                            &NT9KACEN2
 Summary
      Anthracene is  a  three-ringed polycyclic aromatic hydrocar-
 bon (PAH).   It  is probably moderately stable In the environment,
 Anthracene  causes dermatitis  and other  skin disorders in humans,
 CAS Number:   120-12-7
 Chemical Formula:  CJ^HIQ
 I UP AC  Name:   Anthracene
 Important Synonyms and Trade Harness  Paranaphtbalene

 Chemical and  Physical Properties
 Molecular ffeifbti  171.22
 Soiling Points  340 to 355*C
 Meltinf fointi  217*C
 Specific Gravitys  1.24 at 27*C
 Solubility in Water*  0.073 me/liter at 25*C
 Solubility in Organiesi  Soluble in acetone and benzene
 Log octanel/Water Partition Coefficient!   4.4S
 Vapor  Pressures  1.95xlO~4 mm If at 20*C
vapor  Density i  fi.15

              _F»tt
     Much o£ the information concerning transport and fate
is inferred froa data for polycyclic aromatic hydrocarbons
(PAHs) in general, because specific information  for  anthracene
is lacking.  Rapid, direct photolysis of anthracene  to  quinonas
aay occur in aqueous solution.  Oxidation  is probably too slow
to be a significant environmental process.  The  available data
suggest that volatilisation may be a significant transport
Anthracene
Page 1
October 1965
Preceding page blank

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-------
 photodynaaic response concentration of 0.1 nf/liter is reported
 for the freshwater protozoan 9*rameci ua ea uda tag.  Tnt weighted
 average bioconcentration factor for the edible portion of all
 freshwater and estuarine aquatic organisms consumed by Aaericans
 la 478.


 Regulations and Standards

 Aaeient Water Quality Criteria (DSE?A) *.


      The available data art not adequate for establishing criteria,
 REFERENCES

 INTERNATIONAL AGESCY FOR, RESEARCH OH CANCER (IARC)  1983.
      IARC Wonogrophs on the Evaluation of the Carcinogenic Risfc
      of Chtaicala to Hunans. Vol 32:  Polynuckas Aromatic Compounds,
      Part 1, Chemical, Environmental and Experimental Data.
      World Health Organization,  Lyon, Prance

 HATIOHAL INSTITCTB FOR OCCUPATIONAL SATSTTf AND HALTI (ttlOSB) .
      1984.  Registry of Toxic Effects of Chemical Substances.
      Data Base.  Washington, D.C.  July 1984

 SAX,  N.I.  1975.  Dangerous Properties of industrial Materials,
      4th ed.  Van Nostrand Reinhold Co., New York.   1,158 pages

 fT.S.  EHVZROHKEHTAL PROTECTION AGSNC? (USZJA).  1979.  Water-
      Related Environmental fate  of 129 Priority Pollutants.
      Washington, O.C,  December  1979.  E7A 440/4-79-029

 U.S.  E>TV I RON MENTAL PROTECTION AGENCY (USZPA).  1980.  Aabient
      Water Quality Criteria for  Polynuclear Aromatic Hydrocar-
      bons.  Office of water Regulations-and Standards, Criteria
      and Standards Division, Washington, O.C.'  October 1980.
      SfA 440/5-80-069

 WEAST, R.E., ed.  1981.  Handbook of Chemistry and  Physics.
      Clad ed.  CRC Press, Cleveland, Ohio.  2,332 pages
 Anthracene
 Page 3
 October 1985
Prececfing page blank

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                             ANTIMOHlf
 Summary
     Antimony production has been associated with an Increase
 in.lung cancer  in exposed workers,  An inhalation study using
 rats yielded suggestive evidence that antimony trioxide causes
 lung and liver  tumors, and several antimony compounds were
 autagetiic when  tested using bacterial test systeas.  Feaale
 workers exposed to antimony compounds had an increased incidence
 of gynecological disorders and spontaneous abortionsj similar
 effects were observed in an anlaal study.  Antimony also causes
 cardiovascular  changes in humans and nay daaage the ayocardia.
Background Information

     Antimony exists  in  a variety of chemical forms.  It is
found in any of four  valence state*  (-3, 0, +3, or +5).  In
the environment, stibalte (Sb.S,) is the most common naturally
occurring fora of antimony, although it is also found as the
native metal, as antiaonides of heavy metals, and as antimony
oxides.
CAS Number:  7440-31-0

Chemical Formulai  Sb

IHPAC Namei  Antimony


Chemical and Physical Properties  (Metal)

Atoaic Weighti  121.73

Boiling Pointi  17SO*C

Melting Pointi  €3Q.74*C

Specific Gravity:  6.684 at 2S*C

Solubility in Waters  Insoluble;  some compounds are soluble
Antimony
Page 1
October 1985                                     Q^
 Preceding page blank

-------
 Transport and Fate

      Antiaony is present  as  the  soluble oxide or antiaonite
 (*3)  *«lt in aost natural waters,   in  reducing environaenta,
 volatile atiblne (SbH*) say  be formed.  Stibina is a gaa at
 room  temperature, and'it  is  quit*, solubl*  In water.  However,
 i-t is not stable in aaroble  water's  or  air  and is oxidized to
 fora  Sb203.   Tha foraation of stibine  in bad aadiaanta, which
 uaually provide  a reducing environment, »ay offar a mechanism
 for:-r*mobiliration of  antiaony previously  removed from solution.
 atoaethylatlon processes  resulting  in  tha  formation of volatile
 stibina derivatives may also causa  aoaa reaobllizatlon of anti-
 mony.  Tha extent to which aorption radueas tha aqueous transport
 of antiaony  is unknown, but  it is claar that sorption to elays
 and minerale is  normally  tha most important mechanism resulting
 in tha removal of antiaony froa  solution.  Thara also is a
 possibility  that heavy metala in solution  could react with
 •ntiaonita or antimonata  (+3) to fora  insoluble compounds.
 Tha importance of such processes is unknown, but it is likely
 that  aost species of antiaony in natural waters are soluble
 and quite aobile and are  eventually transported in solution
 to the oceans.  Bioaecumulation  appears to be only a ainor
 fate  process for antimony.  Airborne transport of antiaony
 in the fora  of partieulates  can  also occur.


 Health iffects

      Antimony production  has been associated with an increase
 in lung cancer among exposed workers*  ani  one inhalation study
 in rats also indicated that  antiaony trioxid* might produce
 lung  and liver tuaors.  Several  studies in bacterial test ays-
 teas  report  that various  antiaony compounds, including antimony
 trioxide,  antiaony trichloride,  and antimony pentachloride,
 aay be mutaganic.   Reports of effects  on reproduction are limited,
 Afflong the  effects on reproduction reported for humane are impair-
 ment* to the faaala reproductive ayataa.   Feaale workers exposed
 to metallic  antiaony dust, antiaony trioxide, and antiaony
 pentoxide  had an increased incidence of gynecological disorders
 and* late" spontaneous abortions*  Antiaony  was found in toe
 breast ailk,  placantal tissue, aaniotie fluid, and blood of
 the uabilical cord in  exposed workers.  Decreased weight gain
 was obaarvad in  children  born of workera exposed to antiaony.
 The saae paper reports •  study in which intrsperitoneal adaini«
 •tration of  antimony produced changes  in rats that support
 toe findings of  huaan  reproductive  effects.

      Cardiovascular changes  associated with exposure to anti-
aony  represent a serious  health  effect.  Exposure to either
 trivalant  or  pentavalent  antimonial compounds can produce electro-
 cardiofraa (EGG)  changes  in  huaans. Hiatopathological evidence
Antiaony
Page a
October 1983                    .
                                                                    jr

-------
of cardiac edema, myoeardial fibrosis, an<3 other signs of rayoear-
dial structural damage indicates that antimony nay product
even more seven, possibly permanent myocardial damage in humans.
Parallel findings of functional changes in ICG patterns and
of histopathological evidence of rayocardlal structural damage
have also been obtained in animal toxicity studies.  Pneumoconiosis
in response to inhalation exposure and dermatitis in response
to skin exposure have also been observed among individuals
exposed to antimony or its compounds.


Toxicity to Wildlife and Domestic Animals

     Testa with antimony potassium tartrate and antimony tri-
chloride in Daohnia magna reveal no difference in the toxicity
of these two compounds.  The LC-0 and £C«Q values for Paphnia
magna and the fathead minnow, bach freshwater species, range
tSrom 9,000 to 21,900 ug/liter.  Chronic values for the fathead
minnow and paphnia maqna are 1,600 and 5,400 gg/liter, respectively,
Acute-chronic ratios cor the fathead minnow and Paphnia magna
are 14 and 3.S, respectively.  The freshwater alga Selenaatrurn
capricornuturn is more sensitive than the animal* species tested,
witn a 96-nour IC5fl of 110 ug/liter for inhibition of the synthesis
of chlorophyll a.  So detectable bioconcentration of antimony
by the bluegill~was observed.  No definitive data concerning
the toxicity of antimony to saltwater species or to other wildlife
or domestic animals ace available.


Regulations and Standards

Ambient Water Quality Criteria  (USEPA):

     Aquatic Life

     The available data are not adequate for establishing criteria.
     However, EPA did report the lowest values known to be toxic
     in aquatic organisms.

     Freshwater

         Acute toxicityt  9,000 ug/liter
         Chronic toxicityt  1,€00 ug/liter

     Saltwater

         Acute toxicity:  No available data
         Chronic toxicityi  No available data

     Human Health

     Criterion:  146 wg/liter


Antimony
Page 3
October 19IS

-------
 NIOSR  Recommended Standard:  0.5 mg/m  TWA  (antimony
                                  and all antimony compounds
                         .         eieept stibine)
 OSHA Standards   0.5 mg/mj TWA

 ACCIH  Threshold  Limit Valuet  0.5 «g/«3 TWA  (antimony and its
                              coapound* aa Sb)


 REFERENCES

 AMERICAN  CONFERENCE OF GOVERNMENTAL  INDUSTRIAL HYGIBHISTS (ACGIH)
     1980.  Documentation of the Thriahold Limit Values.  4th
     td.  Cincinnati/ Ohio.  481 page*

 NATIONAL  INSTITUTE FOR OCCUPATIONAL  SAFETY AND HEALTH (NIOSH).
     1913.  Registry of  Toxic Effects off Chemical Substances.
     Data Base.  Washington, D.C.  October 1983

 NATIONAL  INSTITUTE FOR OCCUPATIONAL  SAFETY AND HEALTH (NIOSH).
     1978.  Criteria for a Recommended Standard--0ccupational
     Exposure to Antimony.  September 1978.  OHEW Publication
     NO.  (NIOSH) 78-216

 U.S. ENVIRONMENTAL PROTECTION ASENOT (USEPA).  1979.  Water-
     Related Environmental Fate of 129 Priority Pollutants.
     Washington, B.C.  December 1979.  EPA 440/4-79-029

 U.S. ENVIRONMENTAL PROTECTION ASENC* (USEPA).  1910.  AflbUnt
     Water Quality Criteria for Antimony.  Office of Water
     Regulations and Standard*, Criteria and Standards Division,
     Washington, D.C.  October 1980.  EPA 440/5-80-020

 WEAST, R.E., ed.  1981.  Handbook of Chemistry and Physics.
     62nd ed.  CRC Press, Cleveland, Ohio.   2332 pages
Antimony
Page 4
October 1985
                                                                  ,J

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                             ARSENIC
     Arsenic is a metal that Is present in th* environment
as a constituent of organic and inorganic compounds; it also
occurs in a number of valence states.  Arsenic is generally
rather mobile in the natural environment, with th* degree of
nobility dependent on its chemical torn and th* properties
of the surrounding medium.  Arsenic is a human carcinogen;
it causes skin tumors when it is ingested and lung tumors when
it Is inhaled.  Arsenic compounds ar* teratogenic and have
adverse reproductive effects in animals.  Chronic exposure
to arsenic is associated with polyneuropathy and skin lesions.
It is acutely toxic to son* early lif* stages of aquatic organisms
at levels as low as 40 ug/lit*r«
Backg roun d In forma t i on

     Arsenic can be found in th* environment in any of four
valence states  (-1, 0, +3, and +5) depending on th* pH, Eh,
and other factors.  It can exist as either inorganic or organic
compounds and often will change forms as It moves through the
various media.  Th* chemical and physical properties depend on
th* state of th* metalloid.  Only th* properties of metallic
arstnic have been listed; properties of other arsenic compounds
ar* often quit* different.

CAS Number*  7440-38-2

Chemical formulat  A*

IUPAC Name*  Arsenic


Chemical and Physical Properties

Atomic Heighti  74.91

Boiling Point!  613-C

Melting Pointi  817*C

Specific Gravityt  S.72 at 20*C
Arsenic
fag* 1
October 1085

-------
 Solubility in  watert   Insoluble; some salts are soluble


 Transport and  fate

      In the natural environment, arsenic has four different
 oxidation states, and  chemical speoiation is important in deter-
 mining  arsenic's distribution and nobility*  Interconversions
 of  the  4-3 and  4-5 states as well as organic complexation, are
 the,most important.  Arsenic is generally quite mobile in the
 environment.   In the aquatic environment, volatilization is
 important when biological activity or highly reducing conditions
 produce arsine or Bethylarsenies.  Sorption by tbe sediaent
 Is  an Important fate for the chemical.  Arsenic is metabolized
 to  organic arsenicals  by a number of organism*; this Increases
 arsenic's mobility  In  the environment.  Because of its general
 mobility, arsenic tends to cycle through the environment.
 Its ultimate fate is probably the deep ocean, but It may pass
 through numerous stages before finally reaching the sea.


 Health  Effects

      Arsenic has been  Implicated in the production of skin
 cancer  in humans.  There is also extensive evidence that Inha-
 lation  of arsenic compounds causes lung cancer in workers.
 Arsenic compounds cause chromosome damage in animals, and huaana
 exposed to arsenic compounds nave been reported to have an
 elevated incidence of  chromosome aberrations.  Arsenic compounds
 have  been reported to  be teratogenic, fetotoxic, and embryotoxie
 In  several  animal species, and an increased incidence of multiple
 malformations  among children born to women oecupationally exposed
 to  arsenic baa been reported.  Arsenic compounds also causa
 noncancerous,  possibly precancerous, skin changes in exposed
 individuals.   Several  eases of progressive polyneuropathy in-
 volving motor  and sensory nerves and particularly affecting
 the extremities and myelinated long-axon neurons nave been
 reported in individuals oecupationally expoaed to Inorganic
 arsenie.   folyneuropathles have also been reported after the
 Ingestion of arsenic-contaminated foods.


Toxieity to wildlife and Oomestte Aniaals

     Various Inorganic forms of arsenic appear to have similar
levels  of  toxieity; they all seem to be much more toxic than
organic forms.  Acute  toxieity to adult freshwater animals
occurs  at  levels of arsenie trloxide as low as 112 ug/llter
and at  levels  as low as 40 ug/llter In early life stages of
aquatic organisms.  Acute toxieity to saltwater fish occurs
at  levels  around 15 ing/liter, while some invertebrates are
affected at much lower levels (508 Mi Alter).  Arsenie toxieity


Arsenic
f age 2
October 1SS5

-------
 does not appear  to increase  greatly  with  chronic exposure,
 and it does not  seem that  arsenic  is bioconcentrated  to a great
• degree.

      Arsenic poisoning is  a  rare but not  uncommon toxic syndrome
 among domestic animals.  Arsenic causes hypereaia and edema
 of the gastrointestinal  tract,  hemorrhage of the cardiac serosal
 surfaces and peritoneum, and pulmonary congestion and edema;
 and it may  cause liver necrosis.   Information on arsenic toxicity
 to terrestrial wildlife  was  not reported  in the literature
 reviewed,


 Regulations and  Standards

 Ambient Water Quality Criteria  (USEPA):

      Aquatic Life

      Freshwater

         Acute toxicity:   440 ug/litec
         Chronic toxicity:   No  available  data

      Saltwater

         Acute toxicity:   508 ug/liter
         Chronic toxicity:   Ho  available  data

      Human  Health

      Estimates of the carcinogenic risks  associated with lifetime
      exposure to various concentrations of arsenic in water
      are:

      Risk                            Concentration

      10"!                            22 nf/liter
      10 ;                            2.2 ng/liter
      10~7                            0.22  ng/liter

 CAG Onife Risk (USEPA)i  15 (ag/kg/day)"1

 National Interim Primacy Drinking  Water Standard  (OSEPA): *
 50 pg/liter

 NIOSH Recommended Standard (air)i  2 ug/a3 Ceiling Level

 OSHA Standard (air):   500  ng/a3 TWA

 ACGIH Threshold  Limit Value: 200  Mg/a3  (soluble compounds,
 as As)


 Arsenic
 Fage 3
 October 198S

-------
 AMERICAN  CONFERENCE Of GOVERNMENTAL INDUSTRIAL HYGIENISTS  (ACGIH).
      1980.  Documentation of the Threshold Limit Values.   4th
      •d.  Cincinnati/ Ohio.  488 pages

 INTERNATIONAL AGENCY FOR RESEARCH ON CANCER  (IARC).  1980.  An
      •valuation of chemicals and induatrial processes associ-
      ated with cancer in humans based on human and anlaal  data.
      IARC Monographs Volumes 1 to 20.  Cancer Res. 40:1-12

 NATIONAL  INSTITUTE FOR OCCUPATIONAL SAFETY AND HEALTH  (NIOSH).
      1983.  Registry of Toxic Effect! of Chemical Substances.
      Data Base.  Washington, D.C.  October 1983

 U.S.  ENVIRONMENTAL PROTECTION AGENCY  (USE?A).  1979.  Water-
      Related Environmental Pate of 129 Priority Pollutants
      Washington, D.C.  December 1979.  EPA 440/4-79-029

 O.S.  ENVIRONMENTAL PROTECTION AGENCY  (DSEPA).  1980.  Ambient
      Water Quality Criteria foe Arsenic.  Office of Water  Regu-
      lations and Standards, Cclteria and Standards Division,
      Washington, D.C.  October 1980.  BPA 440/5-80-021

 O.S.  ENVIRONMENTAL PROTECTION AGENCY  {DSEPA).  1984.  Health
      Effects Assessment foe Arsenic.  Environmental Criteria
      and Assessment Office, Cincinnati, Ohio,  September 1984.
      ECAO-CIN-I020  (Final Draft) .

 O.S.  ENVIRONMENTAL PROTECTION AGENCY  (OSEPA).  1985.  Health
      Assessment Document for Dichloroaethane  (Methylene Chloride).
      Office of Health and Environmental Assessment.  Washington,
      D.C.  February 1985.  SPA 600/8-82/004F

 WEAST, R.E., ed.  1981.  Handbook of Chemistry and Physics.
      62nd ed.  CSC Press, Cleveland, Ohio.  2,332 pages
Arsenic
page 4
October 198S

-------
                             ASBESTOS
Summary

     Asbestos is a collective tern applied to numerous fibrous
mineral compounds off natural origin.  These compounds are quits
stable in the environment and nay move either by wind dispersion
or* by being transported in surface water.  Asbestos is a human
carcinogen and causes lung- tumors and aesotbelioaas in persons
exposed by inhalation*  Asbestosis, a progressive/ irreversible
lung-'disease is also caused by exposure to asbestos fibers.
Background Information

     Asbestos is a collective mineralogical tern applied to
numerous fibrous mineral silicates composed of silicon, oxygen,
hydrogen, and aetal cations such as sodim, magnesium, calcium,
and iron.  There are two major groups of asbestost  serpentine
(chryaotile) and amphibole  (amosite, crocidolite, anthophyllite,
trenolite, and actinolite).  The chemical composition of dif-
ferent asbestos fibers varies widely, as do the physical and
chemical properties.  Asbestos fibers ace resistant to fire
and to most solvents, but they will deteriorate rapidly in
some reagents (strong acids and bases) at temperatures greater
than about 95 to 100»C.

CAS Numbers  1332-21-4


Transport and fate

     Asbestos is stable and la not prone to significant chemical
or biological degradation in the aquatic environment.  After
introduction into surface waters, it remains  In suspension
until physical degradation or chemical coagulation allows it
to settle into the sediment layer.  The importance of transport
from the surface of aquatic environments by wind-activated
aerosol formation is not known.  However, mobiliiation of asbestos
from terrestrial surfaces and soils into the  ataosphere by
wind is known to occur.  Of 243,S27 Metric tons of asbestos
discharged to the environment in the United States in 1975,
98.31 was discharged to land, LSI to air, and 0.21 to water.
Asbestos
Page 1
October 1985

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 Health Effects

      Th« ••verity ol health effect* associated with asbestos
 depends on several factors including fiber length and diameter,
 the number of fibers, fiber degradation and retention, and
 asbestos type.  The relative pathogenicity o£ asbestos fibers
 wi.th different characteristics appears to be variable*  However/
 all asbestos produces adverse health effects, and therefore,
 it is generally considered as a single entity.
     *
      Asbestos.is a recogniied hunan carcinogen causing lung
 cancer and mesothelloma, a fora of neoplasm of the lining of
 the chest and abdominal cavities, in workers exposed by inhala-
 tion.  Mesothelioaas have also been identified in individuals
 living near asbestos plants.  Excesses of cancers of the gastro-
 intestinal tract have been identified in asbestos-exposed workers;
 it is unclear if exposure is via ingestion or via the passage
 of phagocytized particles through the body from the lung.
 Cancer of the larynx has also been associated with exposure
 to asbestos.  Cigarette smoking potentiates the risk of lung
 cancer in individuals exposed to asbestos.  All commercial
 foras of asbestos are carcinogenic in experimental anlaals.

      Ro data exist on the teratogenicity of asbestos, although
 transplacental transfer of asbestos has been reported,  in
 a study using several chrysotile and crocidolite saaples, both
 transformation of morphology and positive genetic responses
 resulted fron passive inclusion of asbestos In the culture
 aedia of Chinese hamster cells* although very fine fibrous
'glass produced the same abnormalities.  Ho mutagenicity has
 been observed in any bacterial test systeas.

      Long-term exposure to asbestos dust also causes asbestosis,
 a progressive, irreversible lung disease characterised by diffuse
 interstitial fibrosis*  Acute effects are of little consequence
 after exposure to htgh concentrations via Inhalation although
 some temporary breathing difficulty has occasionally been re-
 ported by workers.  Although human data on initial changes
 are unavailable, local inflammatory lesions are found in the
 terminal bronchioles of tats following inhalation.  Progressive
 fibrosis follows within a few we*ks of the direct exposure
 to dust.  In experiments with rats, cellular proliferation
 and DNA synthesis in the stoaach, duodenua, and Jejunua appear
 to be an iaaedlat* response to asbestos ingestion.  Structural
 changes la the ileua, particularly the villir are also observed.


 Toxicity to Wildlife and Ponestie Animals

      No data concerning the effects of asbestos on wildlife
 and domestic aniaals are available.  Tissue saaples of freshwater
 fish  species froa water with known asbestos contamination contain


 Asbestos
 Page  2
 October  1985

-------
asbestos fibers Identical to those in the water.  Muscle tissue
concentrations were about one-twelfth of the average water
concentrations, but liver and kidney fiber concentrations were
500 tines greater than muscle tissue concentrations.


Regulations and standards

Aabient Water Quality Criteria  (USEPA):

     Aquatic Life

     The available data are not adequate for establishing criteria.

     Human Health

     Estimates of carcinogenic risks associated with lifetime
     exposure to various concentrations of asbestos in water
     are;

     Risk               ,         Concentration

     10"!                        300,000 fibers/liter
     10~S                        30,000 fibers/liter
     10                          3,000 fibers/liter

NIOSR Recommended Standards:

     0.1 fibers/ml as an 8-hr TWA
     0.5 fibers/ml as a 15-ain Ceiling Level

OSHA Standards*

     2 fibers longer than 5 MS in length per al of air as an
     8-hour TWA
     10 fibers/111 as a 10-ain Ceiling Level

ACGIH Threshold Limit Valutas

     Anosite, 0.5 fibers greater than 5 pa in length/ml

     Chryiotile, 2 fibers greater than 5 pa in length/ml

     Crocidolite, 0.2 fibers greater than 5 pa in length/ml

     Other torsi, 2 fibers greater than 5 pa in length/ml

     Asbestos is considered a recognized human carcinogen.
Asbestos
Page 3
October 1985
                                                         Aeeoc»«

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 REFERENCES

 AMERICAN CONFERENCE OF GOVERNMENTAL INDUSTRIAL HYGIENISTS  (ACGIH).
      1980.  Documentation of tht Threshold Limit Values.   4th
      •d.  Cincinnatif Ohio.  488 pages

 INTERNATIONAL AGENCY FOR RESEARCH ON CANCER (IARC).  1977.
      IARC Monographs on the Evaluation of the Carcinogenic
      Risk of Chemicals to Nan.  Volume 14s  Asbestos.  World
      Health Organization, Lyon, France

 LEMEN, R.A., DEMENT, J.M., and WAGONER, J.I.  1980.  Epidemiology
      of asbestos-related diseases.  Environ. Health ferspect.
      34:1-11

 NATIONAL INSTITUTE FOR OCCUPATIONAL SAFETY AND HEALTH (NIOSH).
      1983.  Registry of Toxic Effects of Chemical Substances.
      Data Base.  Washington, B.C.

 SCHNEIDERMAN, M.A., NISBET, I.C.T., and BRETT, S.N.  1981.
      Assessment of risks posed by exposure to low levels of
      asbestos in the general environment.  BGA-Berichte 4:
      3/1-3/28

 U.S.  ENVIRONMENTAL PROTECTION AGENCY (USEPA).  1979.  Water-
      Related Environmental Fate of 129 Priority Pollutants.
      Washington, D.C.  December 1979.  EPA 440/4-79-029

 U.S.  ENVIRONMENTAL PROTECTION AGENCY (USEPA).  1980.  Ambient
      Water Quality Criteria foe Asbestos.  Office of Water
      Regulations and Standards, Criteria and Standards Division,
      Washington, D.C. "October 1980.  EPA 440/5-80-022

 O.S.  ENVIRONMENTAL PROTECTION AGENCY (USEPA).  1984.  Health
      Effects Assessment for Asbestos.  Environmental Criteria
      and Assessment Office, Cincinnati, Ohio.   September  1984.
      SCAO-CIN-H049  (Final Draft)
Asbestos
Page 4
October 198S
                                                                  J

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                              BARIUM
Summary
     In  its pure form, barium is an eitreaely reactive metal
that decomposes in water.  In natural waters it forms Insoluble
carbonate or sulfate salts and is usually present at concentra-
tions of less than 1 ing/liter.  Insoluble forms of barium are
not very toxic; but soluble barium salts are highly toxic after
•cute exposure, and they have a prolonged stiaulant effect
on muscles.  A benign pneureoconiosis, baritosis, can result
from inhaling barium dusts.  The EPA Interim Primary Drinking
Water Standard is 1 nig/liter.


CAS Number:  7440-39-3

Chemical Formula:  Ba

IDPAC Name:  Barium


Chemical and Physical Properties

Atomic Weight:  137.3

Soiling Pointi  1,640'C

Melting Point:  725»C

Specific Gravity!  3.S

Solubility In Water:  Decomposes; combines with sulfate
                      present in natural waters to fora
                      BaSO., which has a solubility of
                      1.6 if/liter at 20*C

Solubility in Organicsi  Soluble In alcoholi insoluble in benzene


Transport and rate

     Bariua la extremely reactive, decomposes in water, and
rtadily forma insoluble carbonate and sulfate salts.  Barium
is generally present in solution in surface or groundwatec
only in trace amounts.  Large amounts will not dissolve because
natural waters usually contain sulfate, and the solubility
of bariua sulfate is generally low.  Barium is not soluble
at more than a few parts per million in wattr that contains
sulfate at more than a few parts per million.  However, barium
sulfate may become considerably more soluble in the presence


Barium
Page 1
October 1§8S

-------
 of  chloride  and  other  anions,  Monitoring programs show  that
 it  is rare to find  barium  in drinking water at concentrations
 greater  than 1 ag/liter.   Atmospheric transport of barium,
 in  the for*  of particulates, can occur.  Bioaccuaulation it
 not an important process for barium.


 Health Effects

      There are no reports  of carcinogenic! ty, mutagenicity,
 or  teratogenicity associated with exposure to bariua or  its
 compounds.   Effects on gametogenesis and on the reproductive
 organs are reported in male and female rats after inhalation
 of  barium carbonate? intratesticular injection of bariua chloride
 affects  the  male reproductive organs.

      Insoluble forms of barium, particularly bariua sulfate,
 are not  toxic by ingestion or inhalation because only minimal
 amounts  are  absorbed.   However, soluble bariua compounds are
 highly toxic in  humans after exposure by either route.   The
 most important effect  of acute barium poisoning is a strong,
 prolonged stimulant action on muscle.  Smooth, cardiac,  and
 skeletal muscles are all affected, and a transient increase
 in  blood pressure due  to vasoconstriction can occur.  Effects
 on  the hematopoietic system and cerebral, cortex have also been
 reported in  humans.  Accidental ingestion of soluble bariua
 salts has resulted  in  gastroenteritis, muscular paralysis,
 and ventricular  fibrillation and extra systoles.  Potassium
 deficiency can occur in cases of acute poisoning.  Doses of
 barium carbonate and bariua chloride of S? ag/xg and 11.4 ag/kg,
 respectively,  have  been reported to be fatal in humans.   Digi-
 talis-like toxicity, muscle stimulation, and effects on  the
 hematopoietic and central  nervous systems have been confirmed
 in  experimental  aniaals.   There ace no adequate aniaal data
 available for  deteraining  the chronic effects of low level
 exposure to  bariua  by  ingestion.                              <

      Baritosis,  a benign pneumoconiosis, is an occupational
 disease  arising  froa the inhalation of bariua sulfate dust,
 bariua oiidt  dust,  and bariua carbonate.  The radiologic changes
 produced la  the  lungs  are  reversible with cessation of exposure.
Other  report* oi. industrial exposure to bariua compounds describe
 pulmonary nodulation with  or without • decrease in lung  function.
Dusts  of bariua  oxid*  are  considered potential agents of dermal
 and nasal irritation.   The biological half-lift for bariua
 is  less  than  24  hours.


Toxieity to Wildlife and Domestic Aniaals

     Adequate  data  for characterisation of toxicity to wildlife
and doaestie  aniaals are not available.
Bariua
Page 2
October 1985
                                                                 J

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 Regulations  and  Standards

 Interim Primary  Drinking Water Standard;  1 mg/liter

 OSHA Standard:   0.5 «g/n   (soluble compounds, as Ba)

 ACGIH Threshold  Limit Value:  0.5 mg/mr  (soluble compounds, as Ba)


 REFERENCES

 AMERICAN CONFERENCE Of GOVERNMENTAL INDUSTRIAL HYC-IENISTS  (ACGXH).
      1980.   Documentation of the Threshold Limit Values.   4th ed.
      Cincinnati, Ohio.  488 pages

 DOULL,  J., KLAASSEH, C.D. , and XMDUR, M.Q., eds.  1980.  Casarett
      and Doull's Toxicology:  The Basic  Science of Poisons.
      2nd ed.  Macaillan Publishing Co.,  Hew York.  778 pages

 NATIONAL ACADEMY OF SCIENCES (HAS).  1977.  Drinking Water
      and Health.  Safe Drinking Water Committee, Washington, D.C.
      939 pages

 NATIONAL INSTITUTE FOR OCCUPATIONAL SAFETY AHD HEALTH  (NIOSH).
      1984.   Registry of Toxic Effects of Chemical Substances.
      Data Base.  Washington, D.C.  July  1984

 SAX,  R.I.  1975.  Dangerous Properties of Industrial Materials.
      4th ed.  Van Noatrtnd Rtinhold Co., Hew fork.  1,258 pages

 U.S.  ENVIRONMENTAL PROTECTION AGENCY (USEPA).  1984.  Health
      Effects Assessment for Barium.  Environmental Criteria
      and  Assessment Office, Cincinnati,  Ohio.   September  1984.
      ECAO-CIN-E021  (Final Draft)

 WEAST,  I.E., ed.  1981.  Handbook of Chemistry and Physics.
      62nd ed.  CRC tress, Cleveland, Ohio.  2332 pages
Barium
Page 3
October 1985

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                             BENZENE
     Benzene is an important industrial solvent and chemical
intermediate.  It ia rather volatile/ and ataospheric photooxi-
dation is probably an important fat% process.  Benzene is a
known human carcinogen, causing leukemia in exposed individuals.
It also adversely affects the hematopoietic system.  Benzene
has been shown to b* fetotoxic and to cause eabryolethality
in experimental animals.  Exposure to high concentrations of
benzene in the air causes central nervous systea depression
and cardiovascular effects, and dermal exposure aay cause derma-
titis.
CAS Nuabers  71-43-2

IUPAC Name:  Benzene

Chemical Formula:  C^I,


Chemi eal and Physi ea.l Properties

Molecular Weight;  78.12

Boiling Point:  80.1*C

Melting Points  5.56«C

Specific Gravity:  0.879 at 20*C

Solubility in Water:  1,780 ag/liter at 2S*C

Solubility in Organics:  Hiscible with ethanol, ether, acetic
                         acid, acetone, chloroform, carbon
                       .  disulfide, and carbon tetrachloride

Log Octanol/Water Partition Coefficient!  1.95-2.13

Vapor Pressure:  75 an Hg at 20*C

Vapor Density:  2.77

Plash Point:  -11.1«C
Benzene
Page 1
October 1985
?«9 •. i  . _ _ _         Preceding page blank

-------
 Transport and rate

      Volatilization appears to be the major transport process
 of benxene Iron surface waters to the ambient air/ and atmos-
 pheric transport of benzene occurs readily (USEPA 1979).   Al-
 though direct oxidation of benzene in environmental waters
 is unlikely, cloud chamber data indicate that it may be photo-
 oxidized rapidly in the atmosphere.  Inasmuch as volatilization
 is likely to be the main transport process accounting for the
 rtmoval of benzene from water, the atmospheric destruction
 of benzene is probably the most likely fate process.  Values
 for benzene's 109 octanol/water partition coefficient indicate
 that adsorption onto organic material may be significant under
 conditions of constant exposure,  lorption processes are likely
 removal mechanisms in both surface water and groundwater.
 Although the bioaccumulation potential for benzene appears
 to be low, gradual biodegradation by a variety of microorganisms
 probably occurs.  The rate of benzene biodegradation may be
 enhanced by the presence of other hydrocarbons.


 Health Effects

      Benzene is a recognized human carcinogen (IARC 1982).
 Several epidemiological studies provide sufficient evidence
 of a causal relationship between benzene exposure and leukemia
 in humans.  Benzene is a known inducer of aplastic anemia in
 humans* with a latent period of up to 10 years.  It produces
 leukopenia and thrombocytopenia, which may progress to pancyto-
 penia.  Similar adverse effects on the blood-cell-producing
 system occur in animals exposed to benzene.  In both humans
 and animals, benzene exposure is associated with chromosomal
 damage, although it is not mutagenic in microorganisms.  Benzene
 was fetotoxic and caused embryolethality in experimental animals.

      Exposure to very high concentrations of benzene [about
 20,000 ppa {66,000 mg/mj)  in air]  can be fatal within minutes
 (IARC 1912).  The prominent signs are central norvous system
 depression and convulsions, with death usually following as
-a  consequence .of cardiovascular collapse*  Milder exposures
 can produce vertigo, drowsiness, headache, nausea, and eventually
 unconsciousness If exposure continues.  Deaths from cardiac
 sensitization and cardiac arrhythmias nave also been reported
 after exposure to unknown concentrations*  Although most benzene
 hazards ere associated with inhalation exposure, dermal absorp-
 tion of liquid benzene may occur,  and prolonged or repeated
 skin contact may produce blistering, erythema, and a dry, scaly
 dermatitis.
Benzene
rage  2
October  19S5
                                                                   J

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Toxicity  to Wildlife and Domestic Animals

     The  lCi0 values for benzene in a variety of  invertebrate
and  vertebrate  freshwater aquatic species range from  5,300 ug/liter
to 386,000 M9/liter  (OSEPA  1980).  However, only  values for
the  rainbow trout  (5,300 ug/liter) were obtained  from  a flow
through test and were based on measured concentrations.  Results
based on  unmeasured concentrations in static tests  are likely
to underestimate toxicity for relatively volatile compounds
like benzene.   A chronic test with Paphnia magna  was  incomplete,
with no adverse effects observed at test concentrations as
high as 98,000  tig/liter.

     For  saltwater species, acute values for one  fish  and five
invertebrate species range  froa 10,900 ug/liter to  924,000 tig/liter,
Freshwater and  saltwater plant species that have  been  studied
exhibit toxic effects at benzene concentrations ranging from
20,000 ug/littr to 525,000  ug/liter.


Regulations and Standards

Ambient Water Quality Criteria  (USEPA):

     Aquatic Life

     The  available data are not adequate for establishing criteria.
     However, EPA did report the lowest concentrations of benzene
     known to cause toxic effects in aquatic organisms.

     Freshwater

          Acute  toxicityj  5,300 ug/liter
          Chronic toxicity:  Ho available data


     Saltwater

          Acute  toxicityt  5,100 ug/liter
          Chronic toxicity:  No available data

     Hunan Health-

     Estimates of the carcinogenic risks associated with lifetime
     exposure to various concentrations of benzene  in water
     ares

                                 Concentration

                                 6.6 nf/littr
                                 0.66  ug/liter
                                 0.066 ug/liter


Benzene
Page 3
October 1985
                                                   [Clement AMOC«t*s
                                */

-------
 CAG Unit  Riafc  (OSEPA) t   2,9xlQ"2  (af/kg/day) "*

 OSHA Standards s   30 af/a! ***
                  75 Bt/a%Cailini L«v«l
                  150  »9/«   10-ain F*ak Laval

 ACGIH Thraaoold  Liait. Valuaai   Suspected human carcinogen
                                30 •§/•; TWA
                                75 Bg/aJ STSL


 REFERENCES

 AMERICAN  CONFERENCE OF GOVERNMENTAL  INDUSTRIAL HYGIENISTS  (ACGIH) .
      1980.   Documentation of tha Tfcre ahold Liait Valuaa.   4th
      *d.  Cincinnati, Ohio.  488 page a

 BRIEF,  R.S., LYNCH, J.,  BERNATH, 7., and 3CALA, R.A.  1980.
      Banztna in  tha workplace.  Aa.  Znd. Byg. Aasoc. J. 41:616-623

 OEAN» B.J.   1978.  Canatic  toxicology of banzana* tola*n«,
              and phanols.  Mutat. Raa. 47:75-97
HAAK, H.L.  1980.  Ezpariacntal drug-inductd aplittic anamia.
     Clin. Baaatol.  9:621-639

INTERNATIONAL AGENCY FOR RESEARCH OH CANCER  (IAJC) .  1974.
     IABC Monographa on tha Evaluation of tba Carcinogenic
     Risk of Cnaaieala to Nan.  Vol. 7s  Sooa Anti-Thycoid
     and Ralated Subataneaat Nitrofurana, and Induatrial Chem-
     icals.  World Haalth Organization, Lyon, Franca

INTERNATIONAL AGENCY FOR RESEARCH OH CANCER  (IARC) .  1980.
     An evaluation of chemicala and induatrial processes associ
     ated with eanear in huaana baaed on hunan and aniaal data.
     IARC Monographa Volume a 1 to 20.  Canear Raa. 40 t 1-12

INTERNATIONAL AGENCY FOR RESEARCH ON CANCER  (IMC).  1982.
     IARC Monographa on tba Evaluation of tha Carcinogenic
     Risk of Cbeaicala to Buaana.  Voluae 29:  Soaa Induatrial
     Cheaicala and Dyea tuffs.  World Haalth Organ! tat ion, Lyon,
     Franca

NATIONAL INSTITUTE FOR OCCUPATIONAL SAFETY AND HEALTH (NIOSB).
     1913.  Rag ia try of Toxic Effects of Cheaical  Subatancas.
     Data Base.  Washington, D.C.  October 1983

0.S. ENVIRONKENTAL PROTECTION AGENCY (DSEPA) .  1979.  Water-
     Related Environaental Fata of 129 Priority Pollutants.
     Wa ah ing ton, D.C.  Deceaber 1979.  EPA 440/4-79-029
Benzene
Page 4
October 1985

-------
 U.S.  ENVIRONMENTAL PROTECTION AGENCY (OSEPA).   1980.   Ambient
      Water Quality Criteria foe Benzene.   Office of Water Regula-
      tion! and Standards,  Criteria and Standard! Division,
      Washington,  D.C.   October 1180.  EPA 440/5-80-018

 U.S.  ENVIRONMENTAL PROTECTION AGENCY (DSEPA).   1984.   Health
      Effects Assessment for Benzene.  Environmental Criteria
      and Assessment Office* Cincinnati,  Ohio.   September  1984.
      ECAO-CIN-H037  (Final Draft)

 U.S.  ENVIRONMENTAL PROTECTION AGENCY (OSE?A).   1985.   Health
      Assessment Document for Chloroform.   Office of Health
      and Environmental  Assessment*  Washington,  D.C.  September
      198S.   EPA 600/8-B4/004F

 WALDRON, B.A.   1979.  Target organs:  Toe blood.  J.  Soc.  Occup.
      Med.  29:65-71
Benzene
Page 5
October 1985

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                            BENZIDIfTE
 Summary
     Bensidine it an aromatic amIn* that can be formed  In th«
environment by the degradation of benzidine-baaed dyes.  It
It rapidly oxidised by metal eattons in natural waters  to fora
radical cations which nay be fairly persistent.  Benzidine
it considered to b« a human carcinogen* epideaiolofieal  studies
show that it causes bladder cancer.  It has also caused  liver
and-bladder tumors in aniaala and it is mutagenic in  bacterial
test systems.  Exposure to bentidine causes noncarcinogenic
liver and kidney damage in aniaals exposed by various routes.
Bentidine is toxic to aouatie life at concentrations  as  low
as 2,500 uf/liter.
CAS Ruaberi  92-87-5

Chemical Formula*  ci2&

TUPAC Naaet  Bensidint

Importart Synonyms and Trade Namesi  p-Benxidine;  4f4**Diaaino-
                                     biphenyl


Chemical and^ fh^sical Pregerties

Molecular Weight!  184.23

Boiling fointi  402«C

Melting Pointi  129*C

Specific Gravityt  1.250

Solubility in Watert  400 »g/liter at  12'C

Solubility In Organicsi  Soluble  in  alcohol  and ether

Log Octanol/Water Partition coefficienti  1.81

Vapor Densityi  C.36
Bensidine
Page 1
October lt8S
                                                          Aaeooatse-
  Preceding page blank

-------
 Transport  and  Pitt

      Til* physical and chemical properties of bensidine suggest
 that  direct  photolysis of this compound probably occurs in
 aquatic systems,  pbotoosidatien and direct interaction with
 •oleeular  oxygen or hydroperoxy radicals probably are significant
 fates for  bensidine.  However, oxidation by the sietal cations
 of  natural waters, such as Pe III, HI  III, and Cu II, is probably
 the aost rapid fate process  in aquatic aysteas*  Hydrolysis
 and-..volatilization do not appear to be important environmental
 fa€e  processes.  Although the moderate log octanol/water parti-
 tion  coefficient of benxidine suggests little potential for
 sorptien by  organic partieulatea, adsorption to clay minerals
 and metal  cation complexes is very rapid and may be the most
 important  environmental transport process for this compound*
 It  is suggested that intercalation of  a bensidine radical-cation
 into  clay  particles may increase its stability in environmental
 waters.  These particles could then become part of the bed
 sediment or  could be transported in surface water systems without
 being detected by most analytical methods for measuring benai-
 dine  levels.   Bioaceumulatien does not appear to be an important
 environmental  process for bensidine*   Benaidine is metabolised
 by  mammals,  and detoxification probably proceeds by acetylation
 of  the amino groups.  Biodegradation by activated sludge may
 contribute slightly to the degradation of bensidine during
 sewage plant treatment.  The extent of micrebial degradation
 of  benxidine in natural waters is unknown.


 Health Bffeets

      Bensidine is considered a human carcinogen.  Spideaiologieal
 studies show a strong association between occupational exposure
 to  benxidine and development of bladder cancer.  Exposure can
 occur  through  ingestion, inhalation* or percutaneous abaorption.
 Bensidine  is also carcinogenic in experimental animals.  Per
 example, oral  exposure produces liver  tumors in the rat and
 hamster, and bladder tumors  in the dog.  Bensidine has been
 shown  to be mutagenia ia a variety of  test systems,  no reports
 on  its teratogenioity of reproductive  effects are available.

      Relatively litte information is available concerning the
 noncarclnogenlo effects of bensidine because most experimental
 work  is concerned with evaluating the  carcinogenic risk of the
 compound,  nausea, vomiting, and possibly liver and kidney
 damage are reported to be possible effects due to ingestion.
 In experimental animals, liver and kidney damage are often
observed after chronic or subehronic exposure by various routes.
Benxidine
Page 2
October IfIS

-------
 Toxicitv  to Wildlife  and Domestic Animals

     Available data indicate that acute toxicity to  freshwater
 aquatic life  occurs at concentrations as low as 2,500 yg/liter
 and  would occur  at lover concentrations among species more
 sensitive than those  tested.


 Regulations and  Standards

 Ambient Water Quality Criteria  (USEPA)t

     Aquatic  Life

     The  available data are not adequate for establishing criteria.

     Human Health

     Estimates of the carcinogenic risks associated with lifetime
     exposure to various concentrations of benzidine in water
     are:

     Risk                        Concentration

     10~!                        1.2 ng/liter
     10 !                        0.12 ng/liter
     10                          0.01 ng/liter


 CAG Unit Risk (USEPA}i  234 (mg/kg/day)"1

 NIOSH Recommended Standard;  Human carcinogen

 OS.HA Standard:  Human carcinogen


 REFERENCES

AMERICAN CONFERENCE OF GOVERNMENTAL INDUSTRIAL HYGIENISTS (ACGIH).
     1980.  Documentation of the Threshold Limit Values.  4th
     ed.  Cincinnati, Ohio.  488 pages

 INTERNATIONAL AGENCY FOR RESEARCH ON CANCER (IARC).  1982.
     IARC Monographs  on the Evaluation of the Carcinogenic
     Risk of Chemicals to Humans.  Vol. 29:  Some Industrial
     Chemicals and Dyestuffs.  World Health Organization, Lyon,
     France.

NATIONAL INSTITUTE FOR OCCUPATIONAL SAFETY AND HEALTH (NIOSH}.
     1984.  Registry  of Toxic Effects of Chemical Substances.
     Data Base.   Washington, D.C.  April 1984

SAX,  N.X.   1975.  Dangerous Properties of Industrial Materials.
     4th ed.  Van Nostrand Reinhold Co., Hew York.  1,258 pages

 Benzidine
 Page 3
 October IftS

-------
    .  ISVIROMKIHTAL PROTECTION AGENCY  (OS1PA).  1919.  Hater-
      Related Environmental Fate of 129 Priority Pollutants.
      Washington, D.C.  December 1979.  ZPA 440/4-79-029

 U.S.  ENVIRONMENTAL PROTECTION AGENCY  (USEPA).  1985.  Health
      Assessment Document  for Dichloronethane  (Methylene Chloride).
      Office of Health and Environmental Assessment.  Washington,
      D.C.  February  1985.  SPA 600/8-82/004F

 VERSCHUEREN, I.  1977.  Handbook of Environmental Data on Organic
      Chemicals.  Van Mostrand Reinhold Co., New York.  659
      pages.

 WEAST, R.S., ed.  1981.  Handbook of  Chemistry and Physics.
      62nd ed.  dC Press, Cleveland,  Ohio.  2332 pages
Banzidina
Page 4
October 1915
                             n

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                        BEN20 (a) ANTHRACENE
     Benzo(a)anthracene  is a  four-ringed polycylic aromatic hydro-
 carbon  (PAH).  It  is  readily  absorbed to organic matter and
 is  probably moderately persistent in the environment,  Benzo(a)
 anthracene is carcinogenic in mice and is reported to be muta-
 genic in several test systems.  Carcinogenic PAHs such as benzo(a)
 anthracene cause imaunosuppeession, and dermal exposure causes
 chronic dermatitis and other  skin disorders.  The very limited
 information on its toxicity to aquatic life indicates that
 benzo(a)anthracene is chronically toxic to fish at concentrations
 of  less than 1,000 tig/liter.
CAS Huaberi  56-55-3

Chemical Formula:  cigHi2

IUPAC Namei  1,2-benzanthracene

Important Synonyms and Trade Namesi   1,2-Benzanthracene? 2,3-Benzo-
                                      phenanthrene; Benzo(b)phenanthrene


CJie_m_i eal _and L Ph_y_si .gal._Properti ei

Molecular Weights  228.28

Melting folntt  1S5-15?*C

Solubility in Water:  O.OOS to 0.014  mg/liter at 25'C

Solubility in Organicsi  Soluble in alcohol, ether, acetone,
                         and benzene

Log Octanol/Water Partition Coefficient:   5.61

Vapor Pressurei  5 i 10"9 aa Eg at 20*C


Transport and Fata

     Dissolved benzo(a)anthracene can undergo rapid, direct
photolysis, and this process may be an important environmental
fate in aquatic systems,  studies indicate that singlet  oxygen
is the oxidant and that quinone* §r*  th«  products  in the photo-
iytic reactions.  Ths free-radical oxidation of b*nso(«>anthra-
Benzo(a)anthracene
Page 1
October 1985
                                                 c=*

-------
 cene In th* *nviron»«nt la rapid and may be competitive with
 photolysis- a* a chemical fatt process.   When chlorine and  ozone
 art present in aquatic systems in sufficient quantities, oxid-
 ation reactions resulting in the formation of quinones may
 be significant fat* processes.  Because ben2o(a)anthracene
 does not contain 9roups amenable to hydrolysis,  this  process
 is not thought to be a significant environmental fate.  Vola-
 tilisation does not appear to be an Important transport process
 either.
    *         •
     .Available information Indicates that benzo(a)anthracene
 will' accumulate In th* sediment and biotic portion* of th*
 aquatic environment and that adsorption to suspended  matter
 1* the dominant transport process.  Sorption onto  sediments,
 soil particles, and biota is strongly correlated with the  organic
 carbon level* present.  Although benxo(a)anthracene is readily
 and rapidly bi©accumulated,  it 1* also  rapidly metabolized and
 excreted.   Therefor*,  bioaccumulation is short term and is
 not considered an important  fat* proc*ss.   Benzo(a)anthracene
 is degraded by microbes and  readily metabolised  by multicellular
 organisms.   Degradation by mammals 1* considered to be incom-
 plete;  th*  parent compound and metabolites are excreted by
 th* urinary system.   Biodegradation is  probably  th* ultimate
 fat* process for benzo(a)anthracene. It generally Is nor* rapid
 in soil than in aquatic systems and 1*  relatively  fait In  those
 systems chronically affected by polycyclic aromatic hydrocarbon
 contamination.

      Atmospheric transport of benzo(a)anthracene can  occur/ and
 th* chemical can b* returned to aquatic and terrestrial systems
 by atmospheric  fallout or with precipitation. B*nzo(a)anthra-
 cene  can also enter surface  and groundwater by leaching from
 polluted soils.


 Health  Effects

      Benzo(a)anthracene administered by different  routes is
 carcinogenic in th* sou**.  It can produc* b*patcaias  and lung
 adanoma* following repeated  oral administration  and bladd*r
 tumors  following implantation.  B*nzo(a)anthracan* can also
 produc* tumors  in mice following subcutaneous injections.
Although benzo(a)anthracene  Is a conplete carcinogen  for mouse
 skin,  it produce* less akin  tumors with a longer latency than
 do**  benzo(a)pyrene.   Benxo (a)anthracene ha* not been adequately
 tested  in oth*r sp*cies.

      Benao(a)anthracene i* reported to  b* mutagenic in a variety
 of  t**t systems,   in som* cases, a correlation i*  observed
 between  mutagenicity and carcinogenic potency for  benxo(a)anthra-
 cene  and other  polycyclic aromatic hydrocarbon*.  la  other
word*,  thos* compound* exhibiting greater mutagenic activity


Benxo(a)anthracene
Pag*  2
October  1983

-------
often have higher carcinogenic potency as well.  No adequate
information concerning the teratogenic effects of b«nzo (a)anthracene
in huaans or experimental animals is available,

     Application of the carcinogenic polycyclic aroaatic hydro-
carbons, including benzo(a)anthracene, to souse skin leads
to the destruction of sebaceous glands, hyperplasia, hyperkera-
tosis, and ulceration.  Workers exposed to materials containing
polynuclear aroaatic hydrocarbons aay exhibit chronic dermatitis,
hyperkeratoses, and other skin disorders.  Repeated subcutaneous
injections of benzo(a)anthracene to Bice and rats produces gross
changes in the lyrnphoid tissues.  It has also been shown that
many carcinogenic polycyclic aromatic hydrocarbons can produce
an imnunosuppressive effect/ although specific results with
benzo(a)anthracene have not been reported.


Toxicity to Wildlife and Domestic animals

     Adequate data foe characterization of toxicity to wildlife
and domestic animals are not available.  One study involving
freshwater fish reported an 87% mortality rate in bluegills
exposed to 1,000 gg/liter benzo(a)anthracene for 6 months.


Regulations and Standards

Ambient Water Quality Criteria  (USE?A)t

     Aquatic Life

     The available data are not adequate for establishing criteria.

     Human Health

     Estimates of the carcinogenic risks associated with lifetime
     exposure to various concentrations of carcinogenic PAHs
     in water arei
     Risk                        Concentration
                                 28 ng/liter
                                 2.8 ng/liter
                                 0.28 ng/liter
Benzo(a)anthracene
Page 3
October 198S

-------
 REFERENCES

 AMERICAN CONFERENCE OF  GOVERNMENTAL INDUSTRIAL HYSIBNISTS.
      1180.  Docuaentation  of  tht Threshold Limit Values.   4th
      •d.  Cincinnati, Ohio.   4S8 pages

 INTERNATIONA!. AGENCY fOR RESEARCH ON CANCER  (IARC) .  1973.
      XARC Monograph* on th* Evaluation of Carcinogenic Risk
      of  Chtaieals  to Nan.  Vol. 3i   Certain  polycyclic Aromatic
      Hydrocarbon!  and Heterocyclic  Compounds.   World Health
      Organization,  Lyon, Franc*.  Pp. 45-68

 NATIONAL INSTITUTE  FOR  OCCUPATIONAL SAFETY AND  HEALTH  (NIOSH).
      If83.  Registry of Toxic Effect! of Cheaical  Substances.
      Data Ba«e.  Washington,  D.C.   October 1983

 U.S.  ENVIRONMENTAL  PROTECTION AGENCY (OSEPA).   1979.  Water-
      Related Environmental Pate of  129 Priority Pollutants.
      Washington B.C.   December 1979.  EPA 440/4-79-029

 U.S.  ENVIRONMENTAL  PROTECTION AGENCY (USEPA).   1980.  Aafaient
      Water Quality  Criteria for Polynuclear  Arcaiatic Hydrocar-
      bons.  Office  of Water Regulations and  Standards* Criteria
      and Standards  Division,  Washington, D.C.   October 1980.
      SPA 440/5-80-069

 WEAST, R.E.,  ed.   1981.  Handbook of Chemistry  and Physics.
      62nd Ed.  CRC  Press,  Cleveland, Ohio.   2,332  pages
Benxo{a)anthracene
Page 4
October 1985
                                                                    J

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                          BENZOTHIAZOLZ


Sunnnacv

     Benzothiazole has • aoderate acute toxicity.


CAS. Number:  95-16-9

Chtmical Pornula:  C-H.SCHN

IUPAC Hame:  2-ienzothiazole

Important Synonyms and Tradt Hants:  Benzoaulfonaxole, 0-2857,
                                     l-Thia-3-azaindene» DSAP
                                     BK-4812, and 2-benzothiazole


Chemical and Physical Properties

Molecular Weight:  135.19

Boiling Point:  22?*C

Specific Gravityl  1.246 at 20»C

Solubility in Haters  Slightly soluble in water

Solubility in Organicsi  Freely soluble in alcohol and carbon
                         disulfide

Log Octanol/Wattc Partition Coefficients  2.01


Transport and Fate

     No information on the transport and fate of benxothiazole
was available in the sources reviewed.


Bealth Effects

     Very fev data on the toxicity of benzothiaxole were found
in the literature searched.  The oral ID.* in the mouse is
900 mg/kg, and the intravenous injectionTlD-g value is 95 mg/kg.


Toticity to tfildlife and Oeaestie Animals

     No information on the toxicity of benzothiazole  to wildlife
and domestic animals was found in the sources reviewed.


Benzothiazole
fage 1
October 1985                                      _

-------
REFERENCES

LYMAN, W.J., R1EHL, W.F., and ROSENBLATT, D.I.  1902.  landbook
     of Cheiaical Property Estimation Method*:  Invironaental
     Behavior of Organic Compounds.  McGraw-Hill Book Co.,
     Hew York

THE MERCK INDEX.  1916.  9th ed.  Windholi, M.« ed.  Merck
     and Co., Rahway, H*w J«ra«y

NATIONAL INSTITUTE FOR OCCUPATIONAL SATETY AND EEALTR (NIOSH).
     2.984.  R«gi«try of Toxic Efftetf of Chtmical Subitancta.
     Data Ba»«.  Waahington, D.C.  October 1984

SAX, N.I.  1975.  Dangaroua Prop«rti«§ of Industrial Mattrials.
     4th «d.  Van No»trand R«inhold Co., Ntw York.  1,258 pages

VERSCHOEREN, X.  1977.  Handbook of Environatntal Data on Organic
     Chtaicals.  Van Noatrand Rainhold Co., Hew York.  659 pages

WSAST, R.E., ed.  1982..  Handbook of Ch«ai«try and Phytics.
     62nd ed.  CRC Presa, Cleveland, Ohio.  2,332 pages
Benzothiasole
rage 2
October 19IS

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                            BERYLLX1M
 Summary
     Beryllium  is  a aetal with 4 complicated coordination chem-
 istry,  and  it can  form conplexea, oxycarboxylates, and chelates
 with a  variety  of  materials.  Inhalation exposure to beryllium
 causes  lung and bone cancer in salami*, artd epldemlological
 studies suggest that it Bay cause lang cancer In huaans.  Acute
 respiratory effects are associated mith inhalation of beryllium,
 and dfermal  exposure can cause contact dermatitis.  Chronic expo-
 sure to beryllium  vas reported to have adverse effects on aquatic
 organisms at levels as low as 5.3
CAS Humberi   7440-41-7

Chemical Formula*  Be

IOPAC Haaei   Beryllium


Chemical and  Physical Properties  (Beta!)

Atonic Weights  9.012

Boiling fointi  2970*C

Melting Pointi  137S*C

Specific Gravity:  1.85 at 20*C

Solubility in Waters  Insoluble; aost salts ace soluble

Solubility in Organic*!  Soluble  in dilute acid and alkali»
                         insoluble ia alcoholf etherf and


Transport and fate            f
     Most eoamoa beryllium coapoonds are readily soluble  ia
water.  However, in. water, soluble beryllium salts are hydro-
lyied to for» beryllium hydroxide.  The solubility of beryllium
hydroxide ia quits low  (2 mg/liter) in the pH range of most
natural waters.  Formation of hydrated complexes may increase
the solubility of beryllium somewhat, especially at higher pB
where polynuclear hydroxide complexes may form,  ft is probable,
however, that in sost natural aquatic environments beryllium
is present in particulate rather  than dissolved form.


Berylliua
Page 1
October 19SS

-------
      Although little information  concerning adsorption of  beryl-
 liun is available,  based  on  its geocheaicai similarity to  alu-
 minum it is expected to b* adsorbed  onto  clay mineral surfaces
 at low pB and to be- eoaplaxed  into •one insoluble compounds
 at high pfl.  In -most natural environments, beryllium is likely
 to be present in sorbed or precipitated*  rather than dissolved ,
 fora.

      Beryllium may  be accumulated to a slight extent by aquatic
 orgaoisas.   Although it has  a  low solubility in water, it  is
 possible that benthos could  aecuaulate berylliua froa sediaent
 and thereby transfer the  aetal to higher  organisms  via the
 food chain.  However, there  is no evidence for food chain  mag-
 nification.  Airborne transport of berylliua, generally in
 the fora of participates, aay  also occur.


 Health Effects

      The results  of soae  epideaiological  studies of workers
 oceupationally exposed to berylliua  indicate that beryl! iua
 aay cause lung cancer in  humans.  Although this evidence is
 equivocal,  berylliua and  aany  of  its compounds are  known to
 be carcinogenic in  several animal species.  Inhalation exposure
 to berylliua has  resulted in the  development of lung or bone
 cancer in animals,  and exposure by injection has produced  bone
 cancer.   Although berylliua  compounds aay iapair DHA polymer i -
 sat ion,  there is  no other evidence of autagenic or  clastogenic
 activity*   However, the nuaber of compounds tested  and the
 types of tests conducted  have  been limited.  There  is little
 information concerning the possible  teratogenic effects of
 berylliua.   It is reported to  inhibit embryonic developaent
 of  the snail and  regeneration  of  the limbs of the salaaander.

      Acute  respiratory effects due to berylliua exposure include
 rhinitis, pharyngitis, tracheobroncbitis, and acute pneuaonitis.
 Dermal exposure to  soluble berylliua compounds can  cause contact
 dermatitis.   Ocular effects  include  inflammation of the conjunc-
 tiva  froa splash  burn* or in association  with contact dermatitis.
 The aost coaaon clinical  symptoms caused  by chronic berylliua
 exposure are granuloaatous lung inflammation, with  accompanying
 cough (  chest fain,  and general weakness.  Systemic  effects
 inelud* right neart enlargement with accompanying cardiac  fail-
 ure,  liver  and spleen enlargement, cyanosis, digital clubbing,
 and  kidney  stone  development*


Toitctty to Wildlife and  Domestic Animals

     Data foe several freshwater  fish species indicate that
 the acute toxicity  of beryllium decreases by about  two orders
 of magnitude  with an increase  in  hardness from about 20 to


Beryllium
rage  2
October  1983
                                                                    J

-------
400 mg/liter calcium carbonate.  For example, acut*  values
for th* fathtad minnow rang*  from ISO to 20/000 yg/lit«r over
this tang* of hardness.  Ther* does not appear to b* much vari-
ation  in sensitivity aaong the fish species tested at  similar
levels of hardness.  Acut* and chronic values for the  inverte-
brate  Daphnia aiaqna in th* saae test water  (hardness equal
to 220 at/liter) were reported to be 2,500 and 5.3 jif/llter,
respectively, indicating a very large difference between acute
and chronic toxicity.  Only limited, inconclusive data exist
concerning beryllium toxicity in saltwater species.  Growth
of the green alga Chlorella yannieli is inhibited at a beryllium
concentration of 100,000 pg/liter.A bioconcentration factor
of 19  with a half-life of one day in the whole body  is reported
for the bluegill.

     Some toxicity due to beryllium has been seen in domestic
animals.  One of the earliest observed effects of beryllium
toxicity was the development of rachitic bone changes  after
the addition of soluble beryllium salts to the diet of poultry
and livestock.  Approximately 0.125% beryllium carbonate in
the food or water is required to produce a mild case.


Regulations and Standards

Ambient Water Quality Criteria (USBPA)j

     Aquatic Life

     The available data are not adequate foe establishing criteria,
     However, EPA did report th* lowest concentrations of beryl-
     lium known to cause toxic effects in aquatic organisms.

     Freshwater

          Acute toxicityt  130 ug/llter
          Chronic toxicityi   5.3 M9/liter

     Saltwater

          Acute toxlcity*  Mo available data
          Chronic toxicityt  No available data

     Human Health

     Estimates of the carcinogenic risks associated  with lifetime
     exposure to various concentrations of  beryllium in water
     aret
Beryllium
rage 3
October HtS

-------
      R_lsk                        Concentration

      10~f                        37 ng/liter
      10"";                        3.7 nt/liter
      10"7                        0.37 nf/liter


 CAG  Unit Risk  (USEPA)i   2.6  («g/kg/day)-1

 OSBA Standards  (air)t  2 ug/al TWA
                       5 uf/a^.Ceilinf Level
                       23 Mf/« /30 ain Peak Concentration
ACGIH Threshold Limit Values
REFERENCES
                              Suspected huaan earcinogar
                              2 uf/m3
AMERICAN CONFERENCE OP GOVERNMENTAL INDUSTRIAL BYCIZNISTS (ACGIH).
     1980.  Documentation of the Threahold Li»it Values.  4th
     ad.  Cincinnati, Ohio.  488 pages

NATIONAL INSTITUTE FOR OCCUPATIONAL SAFBTf AND HEALTH  (NIOSH).
     1183.  Registry of Toxic Effects of Che«ical Substances*
     Oats Base.  Haahington, B.C.  October 1983

U.S. ENVIRONMENTAL PROTECTION AGENCY  (DSEPA).  1979.  WatSf-
     Ralatad Envtronaental rat* of 129 Priority Pollutant*.
     Washington, B.C.  December 1979.  EfA 440/4*71-029

U.S. ENVIRONMENTAL PROTECTION AGBNCT  (DSEPA).  1910.  Aabitnt
     Water Quality Criteria foe Berylliua.  Office of Water
     Regulations and Standards* Criteria and Standards Division,
     Washington, D.C. * October 1980.  IPA 440/5-80-024

U.S. ENVIRONMENTAL PROTECTION AGENCY  {DSEPA).  1985.  gealta
     Assessaent Docuaent for Dicbloroaethane (Methylan* Chloride).
     Office of Health sad Bnvironaental Assessaent.  Washington,
     B.C.  february 1985.  HA 600/8-82/004P

WEAST, I.E., ed.  1911.  Handbook of Cheaistry sad Physics.
     62nd ed.  CJtC Press, Cleveland, Ohio.  2332 psgea
Berylliua
Pa§e 4
October 1985
                                9%

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                            1-BOTANOL
 Summary
     1-Butanol, or n-butyl alcohol, is a short-chain alcohol.
 It  is very soluble in water and is likely to ba moderately
 persistent in the environment.  Butanol is irritating to the
 •yea and mucous membranes.  It is not very toxic to aquatic
 life; the lowest dose reported to adversely affect fish was
 1,000 mg/liter in the creek chub.

 CAS. Muaberi  71-3S-3
 Chemical Formula:  C^B^OH
 lapAC N*me:  1-Butanol
 Important Synonyms and Trade Naaest  n-Butanol, n-butyl alcohol,
                                     propyl carbinol
 Chemical and Physical Properties
 Molecular Weight!  74.12
 Boiling Point:  117.7«C
 Malting Point:  -SS.S*C
 Specific Gravity:  0.810 at 20*C
 Solubility in Water:  77,000 »g/liter at 2S*C
 Solubility in Organicsi  Miscible with alcohol, ether, and aany
                         othar organic solvants
 Log Octanol/Water Partition Coefficienti  1.0  (calculated)
Vapor Prtssurai  4.4 u Ig at 20*C
Vapor Dansity»  2.55
 Flash Pointi  3C-38*C

Transport and fata-
     80 information on the transport and fat*  of butanol was
 found in th* sourcas raviawad.  Bowavar, based on the general
 rtactions of alcohols and the specific chemical and physical
1-Butanol
Page 1
Octobar 1985

-------
 properties of the material,  likely  transport  and  fatt process
 can be determined.

      Alcohols ar« very soluble  in water  and therefore prob-
 ably art not very volatile,  although  some evaporation may occur.
 Oxidation is likely to be  an important fate process  in both
 surface water and the  atmosphere.   In soil* butanol  is probably
 biodegtided by soil microorganisms.
 Health Effects

      The  information  on  the  health  effects of butanol  is limited.
 Ho  data on  the  earcinogenieity, mutagenicity, or reproductive
 toxicity  of butanol. were found  in the  literature reviewed.
 Workers exposed to butyl alcohol had greater hearing loss than
 unexposed individuals.   After several  hours of exposure, 600 mg/kg
 of  butanol  irritates  the eyes and mildly  irritates the mucous
membranes  in  humans.
be  710 mg/kg.
The oral LDJO in cats was reported to
Toxicitv  to Wildlife  and Domestic Animals
     The  24-hour
chub were 1,
was toiic to
hour LDD and LD1QO values foe butanol la the c
000 and 1,400 mg/Iiter, respectively.  Butanol
 the alga Ehlorella ovrenoidoea at 8,500 mg/li
                                g/liter.
     Ho  information on the  toiicity of butanol to terrestrial
wildlife or domestic animals was found in  the sources examined.


Regulations and Standards

OSHA Standard  (air)i  300 mg/m3 TWA

ACGIH Threshold Limit Valuei   ISO mg/m3 Ceiling level


8ZFE1ZHC18

AJttRICAS COHTERCTC1 Of GOVIRSHEHTAL IHOnSTHIAL ITGIBWI3T3  (ACGIH)
     1910.  Documentation of the Threshold Limit Values. * 4th
     ed.  Cincinnati, Ohio.  411 pages

AMERICAN ITOOSnilAL IfCZIHi ASSOCIATION  (AIHA).  1978.  Hygitnic
     Guide Series.  Butyl Alcohol  (n-Butanol).  AIHA, Akron,
     Ohio

LTMAN, W.J., IOZHL, V.P., and  ROSENBLATT,  D.I.  1112.  Handbook
     of Chemical Property Estimation Methodsj  Environment*!
     Behavior of Organic Compounds.  McGraw-Hill Book Co.*
     Hew fork

1-Butanol
rage 2
October 1985
                                                                  J

-------
 THE MERCK  IHDEX.   1916.   9th ad.  Windholl, M., ed.  Merck
      and Co., Rahway, New Jersey

 8ATIQNAL IHSTITUTE FOR OCCUPATIONAL SAFETY AND HEALTH  (NIOSH).
      1914.  Registry of Toxic Effect! of Chemical Substances.
      D«t«  Baa*.  Wasbington, B.C.  October 1984

 SAX,  N.I.   1975.   Dangerous Properties of Industrial Materials.
      4th ed.  Van  Nostrand Reinhold Co., Hew York.  1,258 pages

 U.S.  ENVIRONMENTAL PROTECTION ACISC*  COSEFA).  1979.  Water-
      Related Environmental Pate of 129 Priority pollutants.
      Washington, D.C.  Deeeaber 1979.  EPA 440/4-79-029

 VERSCHUEMN, K.  1977.  Handbook of Environaental Data on Organic
      Chemicals.  Van Nostrand Reinhold Co., Mew York.  659 pages

 WEAST, R.E., ed.   1981.   Handbook of Cheaiitry and Pbysies.
      62nd  ed.  CRC Press, Cleveland, Ohio.  2,332 pages
1-Butanol
Page 3
October 1985

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                                         CADMIUM
                 Cadmium is  « metal  that  can  be  present  In  a  variety  of
            chemical  Iotas  in wastes  or  in  the environment.   Some  foras
            are insoluble in water, but  cadmium  is  relatively mobile  in
            the aquatic  environment.   Cadmium is carcinogenic in animals
            exposed by  inhalation  and nay also be in  humans.   It is uncertain
            whether it  is carcinogenic in animals or  humans exposed via
            ingestion.   Cadmium  is a  known  animal taratogen and reproductive
            toxin,  it  has chronic effects  on the kidney, and background
            levels of human  exposure  are  thought to provide only a relative!/
            small margin of  safety for these  effects.


            S ack.grou nd_ I nf oraa t ion

                 Cadmium is  a soft, bluish  whits metal that is obtained as
            a  by-product from the  treatment of til*  ores  of  copper, lead,
            and iron.  Cadmium has a  valence  of  +2  and has  properties similar
            to  those of  zinc.  Cadmium forms  both organic and inorganic
            compounds.   Cadmium  sulfate  is  the most common  salt.

            CAS Mumberi   7440-43-9

            Chemical Formulas  Cd

            IUPAC Samei   Cadmium


            Chenieal and Physical  Properties

            Atomic Weight:   112.41

            Boiling Paint:   7i5*C

            Melting Pointi   321»C

            Specific Gravityt  8.642

            Solubility in Wateri   Salts  are water soluble;  metal  is insoluble

            Solubility in Organics:   Variable, based  on  compound

            Vapor Pressure!   1 mm  Hg  at  3§4*C
           Cadmium
           fage  1
           October 19 B 5
            Preceding page blank

\

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 Transport and fate

      Cadoiurn is relatively aobil* in the aquatic environment com-
 pared to other heavy aetals (USEPA 1979).   It is reaoved from
 aqueous aedia by conpltxing with organic materials and subsequently
 bting adsorbed to the ••dinent.   It appear* that cadmium movts
 slowly through toil/ out only limited information on toil transport
 i* available.  Cadmium uptake by plants is not a significant
 mechanism for depletion of soil  accumulations but aay be signi-
 ficant for human exposure.


 Health Effects

      There is suggestive evidence linking  cadaiua with cancer
 of the prostate in human* (OSEPA 1980).  In animal studies,
 exposure to cadmium by inhalation caused lung tumors in rats,
 and  exposure by injection produced injection-site sarcomas
 and/or teydig-cell tumors (Takenaka 1983,  OSZPA 1981).   An
 increased incidence of tumors has not been seen in animals
 exposed to cadaiua orally*  but four of the five available studies
 were inadequate by current standards (Clement 1983).

      The evidence from a large number of studies on the auta-
 genicity of cadaiua is equivocal, and it has been hypothesized
 that cadmium is not directly autagenie but iapedes repair (Cleaent
 1983).   cadaiua is a known animal teratogen and reproductive
 toxin.   It has been shown to cause renal dysfunction in both.
 huaans and aniaals.   Other toxic effects attributed to cadaiua
 include laaunosuppression (in aniaals), aneaia (in huaans),
 pulmonary disease  (in huaans), possible effects on the endocrine
 system,  defects in sensory function,  and bone daaage.   The
 oral LDSQ in the  rat was 22S ag/kg (NIOSH  1983).


 Toxicity to Wildlife and Ooaestie Aniaals

      Laboratory experiaents suggest that cadaiua aay have adverse
 effects  on reproduction in fish  at levels  present in lightly to
 aoderately polluted waters.

      The acute  LC«Q  for  freshwater fish and invertebrates gener-
 ally ranged  froa  ZOO to 1,000 |ig/literi salaonids are  auch
 more sensitive  than other organisms (USEPA 1960).   Saltwater
 species  were in general 10-fold  more  tolerant to the acute
 effects  of cadaiua.   Chronic tests have been performed and
 show that cadaiua has cumulative toxicity  and acute-chronic
 ratios  that range  of froa €6 to  431.   Bioconcentration factors
 were  generally  less  than 1,000 but were as high as 10 ,.000 for
 some  freshwater fish species.

     Ho  adverse effects on domestic or wild aniaals were reported
 in the studies  reviewed*

Cadaiua
Page  2
October  198S

-------
 Regulation*  and Standards

 Aabitnt Wattr Qutlit* Criteria  (OSEPA) :

     Aquatic Lift  (Proposed 1984}

     Freshwater

         Acute toxicityj  tC1.30tln(hardnessU - 3.92} M/llt,t

         Chronic tOJiicityi  t(0-«tln(b«tdn«««)] - 4.38) Mg/litec

     Saltwater

         Acute toxicity:  38 Mg/liter
         Chronic toxicity:  12  ug/liter

     Hunan Health

     Criterion:  10 pf/liter

CAG Unit Risk for  inhalation exposure  (DSEPA) :  S.I (ag/kg/day) "l

Interim Primary Drinking Water  Standard  (USEPA) :  10 pg/liter

NIOSH Recommended  Standards!  40 ng/a  ,TWA
                              200 |4f/AVlS Bin Ctiling Level
OSHA Standards:  200 ^g/a  TWA
                 600 |ig/m  Ceiling Level

ACGIH Threshold Liait Values:  SO ug/a3 TWA


REFERENCES

AMERICAN CONFERENCE Of GOVERtWENTAL IMDDSTRIAL HYGIENISTS (ACGIH)
     1980.  Docuaentation of the Threshold Liait Values.  4th
     ed.  Cincinnati* Ohio.  4S8 pages

CLEMENT ASSOCIATES, INC.  1983.  Assessment of the Weight of
     Evidence foe Risk Assessment for four Selected Toxic Air
     Pollutants.  Report Prepared for the Air Economic Branch,
     OPRM, U.S. Environmental Protection Agency.  May 1983.

FLEISCHER, M.» SAROFIM/ A. F. , FASSETT, D.W., HAMMOND, P.,
     SCHAKKETTE, H.T. » NISBET, I.C.T., and EPSTEIN, S.  1974.
     Environmental iapact of cadmiumi  A review by the panel
     on hazardous trace substances.  Environ. Health. Pecspect.
     7:253-323
Cadaiua
Page 3
October 1985
                                                             «tee

-------
NATIONAL INSTITUTE FOR OCCUPATIONAL SAFETY AND iEALTS  (MlOSH).
      lfS3.  Registry of Toxic Effects of Cheaieal Substances.
      Beta Base.  Washington, D.C.  October 1983

TAKENAKA, S., OLDICCS, I., KOttIG, H., HOCHRAINER, D.« and
      OBERPORSTER, 6.  1983.  Careinogtnicit/ of cadaiua chloride
      aerosols in W rats.  JNCI 70:367-371

U.S.  ENVIRONMENTAL PROTECTION AGENCY (DSEPA).  1979.  Water-
      ftftlattd Eavironaantal Pat* of 129 Priority Pollutants.
      Washington, D.C.  D*ctab*r 1979.  SPA 440/4-79-029

O.S.  ENVIRONMENTAL PROTECTION AGENCY (OSEPA).  1980.  Ambient
      Water Quality Criteria for Cadmium.  Offie* of Water Regu-
      lations and Standards* Criteria and Standards Division,
      Washington, D.C.  October 1980.  SPA 440/5-80-025

O.S.  ENVIRONMENTAL PROTECTION AGENCY (OSEPA).  1981.  Health
      Assessment Document for Cadaiua.  Environment Criteria
      and Assessment Office.  Research Triangle Park, North
      Carolina.  October 1981.  EPA 600/8-81-023

U.S.  ENVIRONMENTAL PROTECTION AGENCY (OSEPA).  1984.  Health
      Effects Assessment for Cadaiua.  Environmental Criteria
      and Assessment Office, Cincinnati, Ohio,   September 1984.
      ECAO-CIN-3038  (Final Draft)

U.S.  ENVIRONMENTAL PROTECTION AGENCY {DSEPA).  1983.  Health
     Assessment Docuaent foe Chloroform.  Office of Health
      and Environmental Assessment, Washington, D.C.  September
      1985.  EPA 600/8-84/004F
Cadaiua
Page 4
October 198S

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                       CARBON TSTRACflLORIDI
     Carbon  tetrachloride  is  used as an  industrial  solvent
 and  chemical intermediate,  it is an animal carcinogen, causing
 1'iver  tumors in  mice, rats, and hamsters.  Carbon tetrachloride
 also causes  liver  and kidney  damage in aniaals and  humans.
Chemical Formula:

lUPAC.Namet  Tetrachlocoraethane

Important Synonyms and Trade Names:  Tetrachloroaethane, per-
                                     chloromethane


Chemical and Physical Properties

Molecular Weight»  153.8

Boiling Point:  76.7«C

Melting fointt  22.9*C

Specific Gravity:  1.59 at 20*C  (liquid)
                   5.3 vapor (fas) specific gravity

Solubility in Katert  800 mg/liter

Solubility in Organicsi  Miscible with alcohol, benzene, chloro-
                         form, ether, and carbon disulfide

Log Octanol/Water Partition Coefficienti  2.64

Vapor Pressures  90 sa Hg at 20*C

Vapor Densityi  5.32


rranspor tand Fate      s

     Carbon tetrachloride has a high vapor pressure and therefore
volatilises rapidly into the atmosphere froa surface water
and probably froa soil.  Zt Is relatively soluble in water


Carbon tetrachloride
Page 1
October 19S5
                                                             ietee

-------
 and  therefore  would  be  expected  bo  be  transported  In groundwattr.
 Because  of  its high  specific  gravity*  it nay move  independently
 from the groundwater as a  nonaqueous phase  liquid.


 Health Bffeets

      Carbon tetrachloride  was carcinogenic  in mice, rats*  and
 hamsters; in all  eases  liver  tumors were induced  (IARC  1979*
 USEPA 1980.).   In  addition* mice  also displayed a high incidence
 of .tuaors of the  adrenal gland. (Weisburger  197?).  Studies
 discussed by.EPA  (1980)  on the mutagenic and teratogenic effects
 of carbon tetrachloride and its  impact OB reproduction  are
 inconclusive.   Carbon tetrachloride also causes both liver
 and  kidney  damage  in animals  and humans.  One study in  which
 guinea pigs  were  repeatedly exposed to carbon tetrachloride
 vapor for several  months provided evidence  of damage to the
 optic nerve  and degeneration  of  the myelin  sheath  of the sciatic
 nerve (Smyth et al.  1936).


 Toxicity to  Wildlife and Poaestic Animals

     Carbon  tetrachloride  has been  shown to be acutely  toxic
 to aquatic  species at concentrations as low as 35  mg/liter.
 No data  on chronic toxieity to aquatic life were reported  in
 the  literature reviewed*   Pish bioconcentrate carbon tetrachlor-
 ide  by a factor of less than  SO.  Mo studies on the toxieity
 of carbon tetraehloride to domestic animals or terrestrial
 wildlife were  found  In  the literature  reviewed.


 Regulations  and Standards

 Ambient Water  Quality Criteria (USEPA)i

     Aquatic Life

     The available data are not  adequate for establishing  criteria,
     Bowever*  EPA  did* report  the lowest values known to cause
     toxieity  in aquatic organisms.

     freshwater

         Acute toxicityi   33,200 ug/liter
         Chronic toxicityt  Ho available data
                        \
     Saltwatert

         Acute toxieityt   50,000 us/liter
         Chronic toxicityt  Mo available data
Carbon tetrachloride
Page 2
October 1985

-------
     Human Health

     Estimates of the carcinogenic risks associated with lifetime
     exposure to carbon tttrachloride at various concentrations
     In water are:

     Risk                        Concentration

     10"!                        4.0 Pi/liter
     10 *                        0.4 pg/liter
     10                          0.04
CAG Unit Risk  ( USEPA } s  l.SxlO"1  (mg/kg/day)"1

OS HA Standards  (air):  10 ppm TWA
                       25 ppm Ceiling Level


REFERENCES

INTERNATIONAL AGENCY FOR RESEARCH ON CANCER  (IARC).  1979.
     IARC Monographs on the Evaluation of Carcinogenic Risk
     of Chemicals to Buntans.  Vol. 20s  Some Balogenated Hydro-
     carbons.  World Health Organization, Lyon, Prance. Pp. 371-399

NATIONAL INSTITUTE FOR OCCUPATIONAL SAFETY AND HEALTH  (NIOSH) .
     1983.  Registry of Toxic Effects of Chemical Substances.
     Data Base.  Washington, D.C.  October 1983

SMYTH, H.F., SMYTH, B.F., JR., and CARPENTER, C.P.  1931.  The
     chronic toxicity of carbon tetrachloride:  Animal exposure
     and field studies.  J. Ind. Hyg. Toxicol. li: 277-298

a.S, ENVIRONMENTAL PROTECTION AGENCY (USEPA) .  1979.  Water-
     Related Environmental Fate of 129 Priority Pollutants
     Washington, D.C.  December 1979.  EPA 440/4-79-029

D.S. ENVIRONMENTAL PROTECTION AGENCY (DSEPA) .  1980.  Ambient
     Water Quality Criteria for Carbon Tetrachloride.  Office
     of Water Regulations and Standards, Criteria and Standards
     Division, Washington, D.C."  October 1980.  EPA 440/5-80-026

O.S. ENVIRONMENTAL PROTECTION AGENCY (USEPA).  1984.  Health
     Effects Assessment for Carbon Tetrachloride.  Environmental
     Criteria and Assessment Office, Cincinnati, Ohio.  September
     1984.  ECAO-CIN-H039   (Final Draft)
Carbon tetrachloride
Page 3
October 1985

-------
 U.S.  EHVIRONMEHTA1  PROTECTIOK AGENCY  (USEPA) .   1985,  Health
      Assessment  Document  for Dichloroaethane  (Methylene Chloride),
      Offie*  of Health  and Environmental Assessment.  Washington,
      D.C.  February 1985.   EPA  600/8-82/004P

 VTRSCHUER2N, X.   1977.  Handbook of Invironaantal Data on Organic
      Cht»icalf.   Van Koatrand Rtinhold Co., H*w fork.  €59 pages

 WEAST,  l.B., td.  1981.   Handbook of Chamistry  and Physici.
      62nd  «d.  CRC  Pr«as, Clavaland, Ohio.  2,332 pages

 WEISBURGER,  E.K.  1977.   Carcinogenic!ty atudias on halogenated
      hydrocarbons.   Environ. Health Ptrspeet. 21:7-16
Carbon tetrachloride
Page 4
October 1985
                             I/O

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                            CHLORDANB
 Sumnary
      Chlordane  is  an orgahochlorine pesticide that was  formerly
 used  on  field crops and  is presently used to control structural
 pests in homes.  Technical chlordane is a complex mixture that
 Includes two iaoaers of  chlordane, heptachlor, and two  isoners
 of  nonachloc.   it  is very persistent in the environment and is
 strongly bioaccuaulated  in fish and other aquatic organisms.
 Chlord
-------
 Solubility in Wattt:   Proa 0.056 to 1.35 ag/liter  it 2S*C

 Solubility in Organic*:   Miacible in aliphatic  and aromatic
                          eolvents (technical  chlordane}

 Log oetanol/tfater Partition Coefficient!   2.71

 Vapor ?ressurei   1 i  10*' mm Eg  at 20"C  (refined product)

 Flash Points   Miniaua ai*C (technical ehlordane)

             *
 Transport  and Fate

      Chlordane i« very peraiatent in the  environment,  reflating
 chemical and  biological degradation into  harmleaa  substances.
 Chlordane  in  clear water  ia aomewhat volatile,  and thia may  be
 an  important  loaa proceaa.  Leaa loaa of  ehlordane from aquatic
 aysterns occura when organica are present,  and reaidue  concentra-
 tion! in aediment are often much higher than  in water.  There-
 fore,  aorption to aediaent* ia probably important  in removing
 the  cheaical  froa the aquatic environment.  Chlordane  binda
 tightly to aoil particles and peraiats foe years in toil after
 aurfaee application.   However, Chlordane  applied aa an eauisi-
 fiable concentrate ia aore readily volatilised  than when it
 ia applied a* a granular  formulation. Certain  food and feed
 cropa  accumulate  realduea by abaorption froa  the aoil*  Ataoa-
 pherle transport  of vapora  and contaminated duet particlea
 froa aoil  application aitea can  occur.


 Health Effects

     Mixturaa of  cis-chlordane and trans-chlordane produce
 liver  cancer  in aice.  Chlordane also haa autagenic effects
 ia at  least one test  systea.  Reproductive effects,  including
 developaental defects and neonatal aetabolic  and biochemical
 disordera,  are observed in the offspring of aice exposed to
 ehlordane.  Testa with laboratory animala, priaarily rodents,
 deaonstrate acute and chronic toxic effects.  Either isoaer
 alone, or  a mixture of the  two,  appears to exhibit approii-
 aately equal  toxicity.  Acute effects include anorexia, weight
 loss,  treaocs, convulsions, and  death.  Chronic exposure to
 ehlordane  causes  liver changes and induces or suppresses a
 variety of  ensyae systeas*  In addition, ehlordane aay act as
 a cumulative  neurotoxin.  The oral LD.0 in the  rat is  283 ag/kg.
Oxychlordane,  in  epoxide  Metabolite formed froa either ehlordane
 isomer, is significantly  aore acutely toxic than ehlordane.
The  oral LO.Q of  oxychlordane adalniatered to rats in  corn
oil  is If af/kg,  and  it is  43 ag/kg when adainiatered  in an
aqueous suspension.
Chlordane
Page 2
October 1985

-------
     Acute oral or skin exposure to chlordane can cause vomiting,
 seizures, electroeneephalographie dysrhythmia, convulsions, and
 d*ath In humans.  However, most reports of human toxicity are
 inconclusive.  Oxychlordane has been found In a high percentage
 of  human adipose tissue samples and also in human milk samples.


 Toxicity to wildlife and Domestic Animals

     The toxic effects of chlordane art seen at relatively
 low concentrations in some fish and invertebrate species.
 Chlordane also shows strong tendencies foe bioaecunulation in
 some aquatic and terrestrial organisms,  it ean concentrate
 at levels thousands of times greater than the surrounding water
 medium in a variety of aquatic organisms, including bacteria,
 algae, daphnids, and fish.  The EPA criteria for acute exposure
 to freshwater species it 2.4 pg/liter, and it is 0.1? pg/liter
 for chronic exposure.  The corresponding Acute and Chronic
 Values for saltwater species are 0.09 pg/liter, 0.0014 pg/liter,
 and 0.0040  ^g/liter.  The Final Acute-Chronic Ratio Is 14.
 Very little information exists concerning the biotransformation
 of chlordane.  Although biotransformations may be important for
 the ultimate degradation of chlordane, these processes are
 likely to be very slow.

     Chlordane or oxychlordane residues have been found in
 a wide variety of wildlife and domestic animal species, but
 usually at relatively low levels.  Chlordane does not appear
 to be extensively concentrated in the higher members of the
 terrestrial food chain.  Studies indicate that chlordane may
 produce toxic effects in certain soil Invertebrates after surface
 application.  Although little information concerning bioaecunu-
 lation in these organisms is available, the potential bioconcen-
 tration of chlordane or oxychlordane by terrestrial insectivores
 is of concern.  Little information on the toxic effects of
 chlordane to mammalian wildlife and domestic animal species
 is available.  Chlordane or oxychlordane residues have been
 found in crops, meat, fish and poultry, dairy products, and
 eggs.  Oral LD.0 values for chlordane ranging from 331 to 858 pptn
 in the diet {approximately 25-50 mg/kg) are reported for a
 variety of wild bird sp«cies.  Oral LDi0 values ranging from
 100 to 1,000 mg/kg are reported for a variety of animals, including
 rodents, goats, aheap, and chickens.


 Regulations and Standards

Ambient Water Quality Criteria (USZFA)i
Chlordane
Page 3
October 1985
                              1(3

-------
      Aquatic Life

      Freshwater

          Aeutt toaicityt  2.4 pg/Httr
          Chronic toxicityt  0,0043

      Saltwiter

          Acutt toxicity:  0.09 pg/liter
          Chronic toxicity »  0.0040 pg/liter

      Huaan Health

      Istimates of tht carcinogenic risks associated with lifetime
      exposure to various concentrations of chlordane in vater
      ares

      Risk                        Concentration

                                  4.f iig/liter
      10.1                        0.46
      10 '                        0.046 ng/littr

 CAG Unit Risk (USEPA);  1.1

 OSHA Standard (ikin)i  0.5 »g/a3 TWA

 ACGIH Tbf*shold Limit Values (stein )i  0.3 sif/m3 TWA
                                       2 Bf /si3 STK,

 Department of Transportation!  Combustible liquid


 REFEREMC1S

 AMERXCIOf CONPERZNC2 Of GOVEJWMEKTAL INDUSTRIAL H7CI2NISTS ( ACGIH }
      1980.  Documentation of the Threshold Limit values.   4th
      ed.  Cincinnati, Ohio.  4S8 pages

 ATTALLAfl f.B.f WHITAOtt/ D.M.,  and BOO, B.L.  1971.  Comparative
.'     volatility of li
-------
 NATIONAL  RESEARCH COUNCIL OP CANADA.  1974.  ChlordaneI  Its
     Effects on Canadian Ecosystems and its Chemistry.  Subcom-
     •ittt* on Pesticides and Related Compounds Subcommittee
     Report No. 2.  Ottawa, Canada.  Publication No. NRCC 14094
     of til* Environaental Secretariat

 NATIONAL  CANCER INSTITUTE (NCI),  1977,  iloassay of Chlordane
     for  Possible Careinogenicity.  National Cancer Institute
     Careinogenesis Technical Report Series No. 8.  Bethesda,
     Maryland.  DIEW Publication No.  (NIH) 77-808

 U.S. ENVIRONMENTAL PROTECTION AGENCY (BSEPA).  1976.  Draft
     Environmental Impact Statement Concerning Notice of intent
     to Cancel Registered Uses of Products Containing Chlordane
     and  Heptachlor.  Washington, D.C.  August 1976.  EPA
     540/4-76-003

 O.S. ENVIRONMENTAL PROTECTION AGENCY (0SEPA).  1976.  PiStlcidal
     Aspects of Chlordane and Heptachlor in Relation to Man and
     the  Environment—A Further Review, 1972*1975.  Washington,
     D.C.  August 1978.  EPA 540/4-76-005

 U.S. ENVIRONMENTAL PROTECTION AGENCY (USEPA).  1979.  Water-
     Related Environaental fate of 129 Priority Pollutants.
     Washington, B.C.  December 1979.  EPA 440/4-79-029

 9.S. ENVIRONMENTAL PROTECTION AGZNCY (USEPA).  1980.  Aabient
     Water Quality Criteria for Chlordane.  Office of Hater
     Regulations and Standards, Criteria and Standards Division,
     Washington, D.C. * October 1980.  EPA 440/5-80-027

 U.S. ENVIRONMENTAL PROTECTION AGENCY (DSEPA).  1984.  Etalth
     Effects Assessment for Chlordane.  Environaental Criteria
     and Assessaent Office, Cincinnati, Ohio.  September 1984.
     ECAO-CIN-H023  (Final Draft)

 D.S. ENVIRONMENTAL PROTECTION AGENCY (DSEPA).  1985.  Health
     Asstssaent Document for Dichloromethane (Methylene Chloride).
     Office of Health and Environaental Assessaent.  Washington,
     D.C.  February 1985.  SPA 600/8-62/0047

WORTHING, C.R., ed.  1979.  The Pesticide Manual—A World Coapendium,
     British Crop Protection Council, Croydon, England.  655 page*
Chlordane
page 5
October 1985
                                                Ocii

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-------
                              CHLORINE
       Chlorine Is a volatile gas that reacts  In  the  atmosphere
  to product hydrochloric acid,  a strong  acid.  It  la very  reactive
  a.nd therefore is not persistent In the  environment. Chlorine-
  gas is a strong irritant,  and  exposure  to  high  concentrations
  will damage the lungs.   Chlorine,  measured as either total
  resid.ua! chlorine or chlorine-produced  oxidants,  is quite toxic
  to -aquatic organisms.
  CAS tlunberi   7782-50-5

  Chemical  Formula:   Cl


  Chemical  and  Physical Properties

  Atomic  Weight!   35.453

  Soiling Point:   -34.6'C

  Melting Point:   -100.!8*C

  Specific  Gravity*   1.41 (liquid at 20*C)

  Solubility in Water;   Soluble {7.3 g/liter  at  20*C)

  Vapor Pressure:   4,800 ran Hg at 20*C

  Vapor Density:   2.49


  Transport and Pate

      Volatilization of chlorine from aquatic or terrestrial
  systems can occur. In the a biosphere,  chlorine can  react  with
  hydrocarbon*  to  produce HC1» which can  return  to the earth
  with precipitation*  Some researchers suggest  that chlorine
  atoas can act as a catalyst in the degradation of the stratos-
  pheric  esone  layer.

      In water* chlorine Reacts quickly  to fora hypochloroua
  acid  (HOC1),  which is weakly dissociated, and  BC1.   Depending
  on  the  pH level, HOC1, OCl", Cl",  or Cl,  »ay predominate in
  aqueous systems.  Chlorine readily react* with many  types  of
  organic natter and oiidizaole inorganic natter.  Chloroform


  Chlorine
  Page  1
  October 1985
                                                   o*m«nt Aeeeeietee
Preceding page blank

-------
 and other  chlorinated  hydrocarbon* arc known to be formed as
 a  result of  tha  rtactlon of chlorina with humic substances
 and other  organic materials.  Tha prasanea of ammonia or amines
 along  with chlorina can raault  In tha foraation of chloraraines.
 Thaia  co»pounda  generally art much more paraiatant than chlorine,
 hypochlorite, and many chlorinated hydrocarbon!.  In freshwater,
 tha combination  of combined (chloramlnes) and free chlorina
 is 'total  residual chlorine).*   In saltwater, aeveral other
 chlorination products  ara alao  included, and chlorine levels
 are reported aa  "chlorine produced oxidants.*
   •X'

 Health effaeta

     There ara no reports of carcinogenic, teratogenic, or
 reproductive affaeta dua to chlorina exposure in humans or
 experimental animals.  One atudy reported tha oeeurranca of
 chromosomal  aberratlona in cultured human lymphocytes after
 exposure to  chlorina at 60 mg/m .

     As a  gas, chlorina ia extremely irritating to tha mucous
 menbrines  of tha eye*  and respiratory tract.  Acute inhalation
 exposure to  relatively high concentrations can damage tha lunga
 and raault in daeraaaad lung capacity, pulmonary congestion*
 edema, and aometimea death,  other sign* and aymptoma include
 dyspnea and  cough, cyanosis* corrosion of tha teeth, severe
 headache,  nauaea, and  ayncopa.  Experiments with animals confirm
 tha occurrence of irritant affaeta and lung damage as a raault
 of acuta or  chronic exposure to chlorina.  One-hour inhalation
 LC.g valuaa  of 879 ag/ir and 400 mg/m  art reported for the
 rat and mouaa, reapactively.


 Toxieity to  wildlife and Ponestic Animals

     The acuta toxicity of chlorina, measured as total residual
 chlorina (TKC) in freshwater and as chlorine produced oxidants
 (CPO)  In saltwater, ranged from 17 pg/liter to 710 uf/litar for
 31 freshwater apeciea  and from  25 ug/litar to 1*418 ug/litar
 for 23 aaltwatar spaelaSt  Fish and invertebrate species gener-
 ally had comparable rangaa of aanaitivity.  Chronic stadias
 have bean  conducted on 3 frashwater species and 1 aaltwater
 spaeies..   Cbronie values for tha freshwater organisms ranged
 from S to  1? pg/liter, with acute-chronic ratios from 4 to
 20,  Chronic effecta occurred In the aaltwater organism at
 47 pg/litar, and tha acute-chronic ratio for this speciea was
 1.2*

     No information on the toxicity of chlorine to terrastriil
wildlife or  domestic animals was found ia the literature reviewed
Chlorine
Fag* 2 .
October 1983

-------
Regulations and Standards

Proposed Aabient water Quality Criteria (USEPA) :

     Aquatic Life

     Freshwater

         Acute toxicity:  14 Mg/liter
         Chronic toxicity:  8.3 pg/liter

     Saltwater

         Acute toiieityi 13 pg/liter
         Chronic toiicity:  7.4 jjg/liter

NIOSH Recommended Standard:  1.5 ppa

OS HA Standard:  3 »g/a3

ACGIH Threshold Limit Values:  3 «g/»! TWA
                               9 fflf/B4 STEL


REFERENCES

AMEHICAN CONFERENCE OF GOVERNMENTAL INDUSTRIAL HYGXSN1STS (ACGIH),
     1980.  Documentation of the Threshold Limit Values.  4th
     ed.  Cincinnati, Ohio.  4SB pages

DOULL, J.» KLAASSZN, C.D., ArtDUR, M.O., eds.  1980.  Casar-tt
     and Doull's Toxicology;  The Basic Science of Poisons.
     2nd ed.  Macmillan Publishing Co., New York.  778 pages

HATIONAL ACAD1MY OP SCIINCSS (HAS).  1177.  Drinking Water
     and Health,  Safe Drinking Water Committee.  Washington, D.C,
     939 pages

HATIOMAL IH3TITOTO FOR OCCUPAT10SAL SAFETY ASD HEALTH (NIOSR) .
     197$.  Criteria for a Recommended Standard—Occupational
     Exposure to Chlorine.  Washington, D.C*  May 1976.  DHEW
     Publication HO. (NIOSH) 76-170
         1HSTITOTE FOR OCCOPATIONAL SAFETY AMD HEALTH (SIOSH) .
     1984.  Registry of Toxic Effects of Chemical Substances.
     Data Base.  Washington, D.C.  January 1984

SAX, N.I.  1975.  Dangerous Properties of Industrial Materials.
     4th ed.  Van Hostrand Reinhold Co., Hew York.  1,258 pages

TINSL2Y, I.J.  1979.  Chemical Concepts in Pollutant Behavior.
     John Wiley and Sons, New York.  265 pages


Chlorine
Page 3
October 1985

-------
 O.S.  ENVIRONMENTAL  PROTECTION AGENCY  (OSEPA).  1983.  Ambient
      Aquatic  Lift tf«t*r Quality Grit»cia  for chlorine.  Draft
      S«pttmb«r  21,  1183

 KEAST,  K.S.f  «d.  1981.   Bandbook of  Ch«nl»try and  Physics.
      62nd  «d.   CtC  ?r«s»» Cl»v«l«nd,  Ohio.  2332 pag«s
Chlorin*
P»gt 4
October 1983
                                                                  J

-------
                          CHLOROBENZENE
Summary
     Chlorob«nzen« is used as * solvent and a§ a raw material
in chemical manufacturing.  It is persistent In th* environment
and can be adsorbed to organic material in soil*  Chlorobenzene
may cause liver tumors in male mice.  Animals exposed to ehloro-
benzene have exhibited liver and kidney damage.  Chlorobenzene
is not. very toxic to aquatic organisms; none of the LC.n values
are 1'ess than 10 mg/liter.
CAS Number:  108-90-7
Chemical Formulat  C.H.C1
IUPAC Name t  Chlorobenzene
Important Synonyms and Trade Names:  Monochlorobenzene, benzene
                                     chloride, phenyl chloride
Chemical and Physical Properties
Molecular Weighti  112.6
Boiling pointt  131«C
Melting Point:  -46»C
Specific Gravity!  1.11 at 20-C  (liquid)
Solubility in Water:  500 mg/liter
Solubility in Organicsi  Soluble  in alcohol, benzene, chloroform,
                         ether, and carbon tetrachloride
Log Octanol/Water Partition Coefficients  2.83
Vapor Pressure:  8.8 mm Hg at 2Q*C
Vapor Oensityi  3.88
Henry*• Law Constant!  3.56 » lo"3 ata m3/»ol« «t  25*C.
flash Point!  28*C
Chlorobenzene
Page 1
October 1985
                                                  Ciemerw Ammocmtmm

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 Transport  and Fate

      Chlorobenzene  i* probably  reaoved  from  cur fact  water pri-
 marily by  volatilisation,  although adsorption and bioaceuauiation
 say alto be  factor a.  Monochlorobenzene would be expected to
 move slowly  in  aoil because of  its high octanol/water partition
 coefficient  and consequent adsorption to aoil organic material.


 Health Effects

    "•""A atudy.of the carcinogenic! ty of chlorobenzene was recently
 completed  by the National  Toxicology Frograa and preliainary
 results show that chlorobenzene caused neoplastic nodulea in
 the liver  of male rats but was  not carcinogenic in feaale rata
 or  in Bice.

      occupational studies  suggest that chronic exposure to
 raonochlorobenzene vapor nay cause blood dyseraaia, hyperlipide-
 mia,  and cardiac dysfunction in huaana.  Like aany organic
 solvents,  monoehlorobenzene is  a central nervous system depres-
 sant  in overexposed humans, but no chronic neurotoxie effects
 have  been  reported.  Animals exposed to chlorobenzene have
 exhibited  liver and kidney damage and atrophy of the seminiferous
 tubules in the  testes.  The oral LDJO value  for rats was 2910 ag/kg


 Toxicity to  Wildlife and poneatic Animala

      Chlorobenzene  was acutely  toxic to fish at levels greater
 than  25 mg/liter and to aquatic invertebrates at levels greater
 than  10 ag/liter.   Ho chronic studies on the toxicity of chloro-
 benzene to aquatic  life were found in the literature reviewed.
 Monochlorobenzene was shown to  have a bioaccumulation factor
 of  about 1,000  in freshwater species.  No studies on terrestrial
 wildlife or  doaestie animal a were reported in the literature
 reviewed.


 Regulations  and  Standards

Aaeient Water Quality Criteria  (USE? A) i

      Aquatic Life

     Tat available  datavare not adequate for establishing criteria.

     Huaan Health
          Health criterion!  488
          Organoleptic criterion!  20
Chlorobenzene
Page 2
October 1983
                                                                   J

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 OSHA Standard  (air)!   350 «g/«3 TWA

 ACGIH Threshold Limit  V»lu«: 350 «g/*3 TWA
REFERENCES

AMERICAN COUHCIl. OF GOVERNMENTAL INDUSRIAL RYGIENISTS (ACGIH).
     1910.  Documentation of Threshold Limit Values.  4th ed.
     Cincinnati, Ohio.  488 pages

NATIONAL INSTITUTE FOR OCCUPATIONAL SAFETY AND HEALTH (NIQSH).
     1983.  Registry of Toxic Iffacts of Chemical Substances.
     Data Bas*.  Washington, B.C.  October 1983

U.S. ENVIRONMENTAL PROTECTION AGENCY  (OSEPA).  1979.  Water-
     Relattd Environmental Pats of 129 Priority Pollutants.
     Washington, D.C.  D«c«mb«r 1979.  EPA 440/4-79-029

D.S. ENVIRONMENTAJ. PROTECTION AGENCY  (USEPA) .  1980.  Ambient
     Matte Quality Criteria for Chlorinated Benzenes.  Offict
     of Water Regulations and Standardsi Criteria and Standards
     Division, Washington, D.C.  October 1910.  EPA 440/5-80-028

U.S. ENVIRONMENTAL PROTECTION AGENCY  (USEPA).  1980.  Support
     Docunent:  Health Effects Test Rulei  Chlorinated Benzenes.
     Assessment Division, Offie* of Toiie Substances.  Washington,
     D.C.  EPA 560/11-10/014

U.S. ENVIRONMENTAL PROTECTION AGENCY  (USEPA).  1984.  Health
     Effects Assessment foe Chlorobenzene.  Bnvironaental Criteria
     and Assessment Office, Cincinnati, Ohio*   September 1984.
     ECAO-CIN-H040  (Final Draft)

VERSCBUEREN, K.  1977.  Handbook of Environmental Data on Organic
    ' Chemicals.  Van Nostrand Reinhold Co., Haw York.  £59 pages

WEAST, R.E., ed.  1981.  Handbook of Chemistry and Physics.
     62nd ed.  QIC Press, Cleveland, Obio.  2,332 pages
Chlorobenxene
Page 3
October 1915

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                         CHLOROBEN2ILATE
Summary
     Chlotob«nzilate is an organochlorine pesticide used to
control aites.  It is moderately persistent in th« •nvironment,
Chronic ingestion of ehlorobenzilate caused testicular atrophy
in aale rats, enlarged livers in female rats and liver cancer
in several strains of nice.  It is moderately toxic to aquatic
organisms, with acute tosicity valuta as low as 550
CAS Number:  510-15-6

Chemical Formulas  cigHi4C1203

I UP AC Name!  lthyl-4,4-dichiorobenjilate

Important Synonyms and Tradt Names:  Altar, Benzilan, folbex


Chemical and Physical Properties

Molecular Weights  325.2

Boiling Point!  141-142*C at 0.06 oa Hg

Melting Point!  35-37«C

Specific Gravity!  1.2316 at 20*C

Solubility in Haters  Practically insoluble

Solubility in Organics:  Soluble in most organic solvents and
                         petroleum oils

Log Octanol/Water Partition Coefficients  Approximately 5 (calcu-
                                          lated)

Vapor Pressurei  6.8xlO"fi mm Eg at 20*C


Transport and fate

     Little information^ the transport and fate of chloro-
benzilate was found in tine sources reviewed.  However* some
generalisations can be made based on its chemical and physical
properties and on the information available about related chemi-
cals.  Chlorobeniilate appears to be moderately persistent.
Although it has a low vapor pressure, as in the case of other
organochloride compounds, volatilisation is probably an important


Chlorobensilate
Page 1
October 1915
 Preceding page blank

-------
 transport  process.  Th» hifh  log octanol/water partition  coeffi-
 eitnt  indicates  that chlorobensilate is probably readily  iorbed
 by soil  materials and sediment and will not move easily through
 fcoundw«t*r  or surface wattr.  Chlorobensilate has been shown
 to b*  •*tabolis«d in dog« and say therefore be biodegraded by
 oth*r  organisms.  Based on  this information and data on th*
 degradation  of DDT, soil bacteria aay play an important rol*
 in the fate  of ehlorobensilate.


 •ealth Effects

     Chlorobensilate produced hepatocellular earcinoaas in
 both Bales and feaales in one strain of aice (NCI 1978) and
 in Bale  Bice  in  two ether strains (IARC 1983).  A slightly
 increased  incidence of adrenocortical adenoaas was seen in
 rats of  both  sexes, but these data were considered inadequate
 for evaluation by IARC (1983).  Colorobensilate does not appear
 to be  mutagenic  and did not adversely affect reproduction in
 a  three-generation study.

     female rats fed 100 ppa ehlorobensilate (approximately
 5  mg/kg  bw/day)  for 4 weeks developed enlarged livers.  Male
 rats fed 1,600 or 3,000 ppa of calorobensilata (approximately
 135 ag/kg bw/day} for 78 weeks experienced teeticular atrophy.
 The acute oral LD.n value for rats, aice, and hamsters was
 700 mg/kg.       3W


 Toxicity to Wildlife and Domestic Animals

     Rainbow  trout exposed to chlorobenxilate for 41 hours had
 an LCS. value of 710 ug/liter.  A 48-bour LC«Q of 550 ug/liter
 was determined foe water fleas.  Ho other information on the
 toxicity of chlorobenxilate to wildlife or domestic animals
 was found in  the literature reviewed.
REFERENCES

EXECUTIVE OFP1CZ OF THE PRESIDENT.  1171.  Ecological Effects
     of Pesticides on Nontarget Species*  Office of Science
     and Technology, Washington, D.C.  June 1971.  EOP/OST-71

FARM CHEMICAL HANDBOOK.  1914.  70th ad.  Mister, R.T., ed.
     Meister Publishing Co., Willoughby, Ohio

HORN, I.J., 1R0CX, ft.B,» and PATOTUt, O.E.  1955.  Toxicology
     of chlorobenxilate.  J. Agric. rood Chea. 3t752-756

1HTERKATIONAL AGBNCY FOR RESEARCH ON CANCER (IARC).  1103.
     LARC Monographs en the Evaluation of Carcinogenic Risk


Chlorobenxilate
Fage 2
October 1985

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      of  Chtmicali  to Humans.  Vol.  30:  Miscellaneous Pesticides
      World Health  Organization, tyen, France.  Pp.  73-85

 TIE  MERCK XNDIX,   1971.   9th td.  Windhol*, M., «d.  Merck
      and Co., Hallway* New Jtrsay

 NATIONAL CANCER INSTITUTE (NCI).  1978.  Bioassay of Chloroben-
      xilate  for Possible  Carcinofenicity,   (CAS Mo. 510-15-6)
      NCI Carcinogenesis Technical Report Series No. 75.  Wash-
      ington, D.C.  DHEW Publication No. (NIB} 71-1325

NATIONAL INSTITUTE POR OCCUPATIONAL SAFETY AND IEALTH (NIOSH),
      1984.   Registry of Toxic Effects of Chemical Substances.
      Data Base.  Washington, D.C.  October 1984

SAX,  N.I.  1975.   Dangerous Properties of Industrial Materials.
      4th ed.  Van  Nostrand Reinhold Co., New York.  1,258 pages

U.S.  ENVIRONMENTAL PROTECTION AGENCY  (USEPA).  1979.  Water-
      Related Environmental Pate of 129 Priority Pollutants.
      Washington, D.C.  December 1979.  EPA 440/4-79-029

WORTHING, C.R., ed.  1979.  The Pesticide Manuals  A World
      Compendium.   British Crop Protection Council, Croydon,
      England.  655 pages
Chlorobenzilate
Page 3
October 1985

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                           CHLO ROE THANE
Summary
     ChXoco«thane Is u«ed as a solvent, as a refrigerant, and
as a raw Material In the manufacture of tetraethyl lead,  it
is fairly volatile in the environment.  Chloroethane caused
headaches and dizziness in workers exposed to high levels.
It causes kidney damage and liver changes in chronically exposed
animals.
CAS Numbers  75-00-3
Chemical formula:  CjHgCl
I UP AC Nane:  Chloroethane
Important Synonyms and Trade Harness  Ethyl chloride, monochloro-
                                     ethane
Chemical and Physical Properties
Molecular Height:  64.52
Boiling Point:  12.3*C
Meltinf Points  -136. 4*C
Specific Gravityt  0.8978 at 20*C
Solubility in Waters  S740 mg/liter at 20*C
Solubility in Organics:  Soluble In alcohol and ether
Log Octanol/Water Partition Coefficient:  1.54
Vapor Pressures  1,000 »» Eg at 20*C
Vapor Density*  2.23

Transport and Fate
     Chloroethane is probably not very persistent in the  environ-
ment.  It volatilizes rapidly from water; once in the atmosphere,
it is photooxidiied, and formyl chloride is the initial oxidation
product.  Hydrolysis may also occur In surface water or in moist
soil.  Biodegradation, sorption, and bioaccunulation probably are
not important fata processes for Chloroethane.

Chloroethane
Page 1
October 1985
n_
Preceding page blank

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 Health  Effects

     Chloroethane  is  presently  being  tested by  th* national
 Toxicology  Program (HTTP)  foe  eareinog*nlclty and  genetic  toxi-
 city.   No information evaluating  ita  reproductive toxicity
 or  teratogenicity  was found.  Chloroethant caused ainor neuro-
 logical affacti  (e.g., headache,  disxiness) in  worker* exposed
 bo  high levels,  in anlaals,  chronic  exposure to  Chloroethane
 caused  kidney daaage  and  fatty  changes In th* liver, and  at
 high l*v«li upaet  cardiac rhytha.  Monochloro«than« i» considered
 to  b* tha laaat  toxic of  th*  chlorinated tthantt.


 Toxieity to Wildlifg  and  Domestic Aniaala

     No information was found on  th*  toxicity of  chlocoethane
 to  wildlife or domestic animals.  The toxicity  of other chlori-
 nated ethanes to aquatic  organisas generally declines with
 decreasing  chlorine content.  Therefore, chloroethan* is  probably
 less toxic  than  1,2-dichloroethane, which causes  acute toxicity
 at  about 120 ag/liter and chronic toxieity at 20  mg/liter,


 Regulations and Standards

 Anbient ifater Quality Criteria  (OSZPA) s

     The available data were  not  adequate for establishing
 criteria.

 OSHA Standard (air)i   2,800 ag/a3 TWA

 ACGIH Threshold Liait Vainest   2*600  ag/a? TWA
                                3,250  ag/aj STZL


 REFERENCES

 AMERICAN CONrZRIHCl OT GOVBRNMENTAL INDUSTRIAL  HYGIENISTS (ACGIH).
     1980.   Docuaentation of  the Threshold Liait Values*.  4th
     ed.  Cincinnati, Ohio.   488  pages

 NATIONAL INSTITUTE FOR OCCUPATIONAL SAFETY AND  HEALTH (NIOSH).
     1983,   Registry  of Toxic Effects* of Chealcal Substance's.
     Data Base.  Washington,  D.C.  October 1983

 PATTY,  P.A., ed.   1913. "industrial lygiene and Toxicology.
     Vol. 2.  John Wiley  i Sons, Mew  York

 SAX, M.S.   1975.  Dangerous Properties of Industrial Materials.
     4th  ed.  Van Nostrand Reinhold Co., New York
Chlocoethane
Page 2
October 1985
                                                                   J

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      U.S. INVIROMMENtW, PROTECTION AGENC* (USEPA).   1979.   Water-
-\         Related Environmental Fat* of 129 Priority pollutants
           Washington, O.C.  Beeeaber 1979.   EPA 440/4-79-029

      U.S. ENVIRONMENTAL PROTECTION AGENCY (USEPA).   1910.   Afflbi«nt
           Water Quality Criteria for Chlorinated Ethanes.   Office
           of Water Regulations and Standards,  Criteria  and  Standards
           Division, Washington, D.C.  October  1910.   EPA 440/5-80-029

      VERSCHUEREN, K.  19??.   Handbook of Environmental  Data on  Organic
          'Chemicals.  Van Hostrand Reinhold Co., New York.   659 pages

      WEAST,  I.E., ed.  1981,  Handbook of Chemistry  and Physics.
           12nd ed.  CRC Press, Cleveland, Ohio. 2,332  pages
      Chloroethane
      Page 3
      October 1985

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                     BIS(2-CHLOROETHOXY)ETHANE
 Summary
      bis(2-Chloroethoiy)ethane  is probably  somewhat persistent
 in  the  environaent.   It his oral LD-0  values  in rats and guinea
 pigs  of 250 ag/kg  and 120  ng/lcg, respectively.
 CAS Number:   112-26-5 '
 Chemical Formula:  C-Ii-Cl-O-
 IUPAC Name:   1,2-bis-2-Chloroethojtyethane
 Important  Synonyms and Trade Manes:  Triglycol dichloride,
                                     triethylene glycol dichloride
 Chemical and  Physical Properties
 Molecular  Height:  117
 Boiling Point:   241.3*C
 Melting Point:   -31.5'C
 Specific Gravity:  1.2 at  2Q«C
 Solubility in Wateri  Approxiaately  5,000 mg/liter  (calculated)
 Log Octanol/Water Partition Coefficients  1.92  (calculated)
 Vapor Pressure:  Probably  less  than  0.1 am  Hg at 20*C
 Plash Point:  121*C

 Transport  and Fate
      No information is available on  the transport and  fate
 of  bis(2-chloroetho»y)ethane.   However, this  information can
 be  extrapolated  fro*  data  on bi» (2-chloroethoxy)aethane data
 and froa the  cbeaical and-physical properties of bis(2-chloro-
 ethoxy)ethane.
      bis(2-Chloroethoxy)ethane  is probably  rather persistent
 in  the  environment,   zt lias a low vapor pressure and therefore
 probably is not  very  volatile.  Its  calculated log octanol/water
 partition  coefficient (1.92) and solubility suggest that it nay
 leach through the soil if  it is not  biodegraded.  There is no

 bis(2-Chloroethoxy)ethane
 Page  1
 October 198S

Preceding page blank

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 information  on  the  bi©degradation of bis(2-chloroethoay)ethane.
 Eased  on  information for  bis(2-chloroetho*y)aethane, the most
 likely fat*  processes  for bis{2-ehloroetho«y)ethane are slow
 hydrolysis and  oxidation  to peroxides.


 Health Bffteti

     Limited information  Is availablt on the bealta effects
 of  bis(2-chloroetho«y)ethane.  Three acute studies indicated
 that the  chemical had  oral LD-Q values of 250 ag/kg in rats
 and 120 mg/kg in guinea pigs and an LO.Q of 1/410 mg/kg vhen
 applied to the  skin of alee.

     More inforaation  on  the potential effects of bis(2-chloroetho*y)
 ethane can be inferred from studies on bis(2-chloromethoxy)ethane.
 This chemical produced local sarcomas when applied dtrmally,
 by subcutaneous injection, or  intraperitoneally.


 Toiicitv  to  Wildlife and  Poaeatic Animals

     Ho inforaation on the toxicity of bis(2-chloro«thoxy)ethane
 to wildlife  or doaestic aniaals was found in the sources reviewed,


 REFERENCES

 THE CONDENSED CHEMICAL DICTIONARY.  1977.  9th ed.  Van MOStrand
     Reinhold Co.,  Mew York

 INTERNATIONAL AGENCY FOR  RESEARCH OR CANCER (IARC).  1977.
     IARC Monographs on the Evaluation of Carcinogenic Risk
     of Chemicals to Man.  Vol. lit  Soae Puaigants, toe Htrbi-
     cides 2,4-D and 2,4»5-T, Chlorinated Dibeniodioxins and
     Miscellaneous  Industrial Cheaicals.  World Health Organiza-
     tion, Lyon, franc*.  Pp. 31-33

 LYMAN, W.J.,  RIEHLr W.F., ROSE>OLATT, O.i.  1912.  Handbook
     of Chemical Property Estimation Methods:  Bnvironaental
     Behavior of Organic  Compounds.  McGraw-Hill Book Co.,
     New fork

RATIONAL ISSTITUT3  FOR OCCUPATIONAL SAFETY AMD HEALTH (NIOSH).
     1914.   Registry of Toxic Effects of Chemical Substances.
     Data Ease.  Washington, D.C.  July 1984

0.3. ENVIRONMENTAL  PROTECTION AGENCY (USE?A).  1979.  Water-
     Related  Environmental Pate of 129 Priority pollutants.
     Washington, D.C.  December 1979.  IfA 440/4-79-029
bis(2-Chloroethory)ethane
fage 2
October 1985

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                     SIS(2-CHLOROETHYL)ETHER
 Summary
     bis(2-Chloroethyl)ether was used in the past a* • soil
 furaigant  and  is now used as a solvent and eheaical reagent.
 It is  fairly  soluble  in water and is probably moderately per-
 sistent In  the environment,  bis(2-Chloroethyl)ether caused
 an increased  incidence of  liver  tumors in aale nice following
 oral,-administration,  and it was  found to be mutagenie using
 the Ames  assay.   In the air, it  is irritating to th« eyes and
 nasal  passages and when inhaled  can damage the lungs* liver,
 kidneys,  and  brain.
CAS numbers   111-44-4

Chemical Formulas  ClCHjCHjOCH-CHjCl

IUPAC Names   bis(beta-Chloroethyl)ether

Important Synonyms and Trade Namest  sym-Dichloroethyl ether>
                                     2,2*-01chloroethyl ethen
                                     l-Chloro-2-(beta-chloroethoxy)
                                     ethanes DCEEi l,l'-oxybis-
                                     (2-chloroethane)


Chemical andPhysical Properties

Molecular Weights  143.02

Boiling Points   178*C

Melting Points  -24.5*C

Specific Gravityt  1.22 at  2Q*C

Solubility in Waters  10,200 ag/liter

Solubility in Organicst  Miscible with most organic solvents
                                                            *

Log Octanol/Water Partition Coefficients   1.5S

Vapor Pressures  0.71 mm Hg at 20*C

Vapor Densitys   4.93

Plash points  SS*C


bisU-Chloroethyl) ether
Page 1
October 1985

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 Transport  and Fate

     There 1« little  information available concerning  the environ-
 mental  transport and  fat* of bis(2-chloroethyl)ether and the
 relative importance of  tht various transport and fatft  processes,
 Some volatilisation of  tali compound from aquatic and  terrestrial
 systems, and subsequent atmospheric transport probably can
 occur.  lecause it it somewhat soluble in water, bis(2-chloroethyl}
 ether can  migrate through the toil,  Direct photolysis is not
 expected to tak* plae*  in the atmosphere or in surface waters.
 How«v«r, photo oxidation of th* bis(2-ehloroethyl)ether that
 reaches th« troposphere is likely to occur,  slow hydrolytic
 cleavage of th« c«rbon-chlorin« bonds can occur and is probably
 th* most important aquatic fat*.                 /

     Adsorption on partlculat* matttr do«s not appear  to b*
 a significant environmental transport process.  A limited aaount
 of indirect evidence  suggests that bis(2-chloroethyl)ether
 has little potential  for bioaccumulation.  Available information
 is not adequate to characterize the importance of biodegradation
 as a fate  process.  It  is reported that significant degradation
 can occur  in aquatic  systems after a period of acclimation.


 Health Effects

     bis(2-Cbloroethyl)ether caused an Increased incidence of
 hepatoaas  in male mice  following oral administration.  It is
 also reported to be mutagenic in Salmonella tester strains.
 Mo data concerning teratogenic or reproductive effects are
 available.

     bis(2-Chloroethyl)ether concentrations of 100 ppm (€00 mg/m3)
 and possibly lover are  irritating to the eyes and nasal passagest
 and may cause coughing  and nausea.  Exposure to concentrations
 above SSO  ppm (3,300  ag/m°) Is considered to be intolerable.
Concentrations of SOO ppm and 230 ppm are reported to  be fatal
 in guinea  pigs and rats* respectively.  The most severe toxic
effects are seen in the lungs* although the kidneys, liver,
and brain  may also be affected.  HO serious toxic effects were
noted following chronic exposure of guinea pigs and rats to
 69 ppm  (420 mg/m3) of bis(J-cbloroethyl)ether.

     bis(2-Chloroethyl)ether is a mild skin irritant.  However,
acutely toxic and lethal amount* may be absorbed through the
skin.  An  oral LB50 of  75 mg/kg is reported for the rat.


Toxicity to Wildlife  and Domestic Animals

     Data  adequate to characterise the toxicity of bis(2-chloro-
ethyl)ether to wildlife and domestic animals are not available.


bis(2-Chloroethyl)ether
Page 2
October 1985

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Acute toiicity of ehloroalkyl ethers, In general, to freshwater
aquatic lift is reported to occur it concentrations as low
as 238 r 000 HgAiter and would occur at lower concentrations
aaong species aore stnsitivt than those tasted.
                                                  •>

Regulation* and Standard!

Aabient Water Quality Criteria (DSEPA) :

     Aquatic Life

     The available data are not adequate for establishing criteria.

     Human Health

     Estimates of the carcinogenic risks associated with lifetime
     exposure to various concentrations of bis (2-chloroethyl) ether
     in water are:

        Risk                •     Concentration
        IQ                       0.3
        10 ,                     0.03 Mg/liter
        10                       0.003 pg/littr

CAG Unit Risk  (USEPA)s  1.14  (ag/kg/day } ~ *

OSHA Standard:  §0 ag/a3 Ceiling Level

ACGIH Threshold Limit Values:  30 ag/a? TLV
                               SO ag/a  STEIi


REFERENCES

AMERICAN CONFERENCE Of GOVERNMENTAL INDUSTRAL HYGIENISTS (ACGIH)
     1980.  Documentation of the Threshold Limit Values.  4th
     Ed.  Cincinnati, Ohio.  488 pages

INTERNATIONAL AGENCY FOR RESEARCH ON CANCER (IARC) .  1975.
     IARC Monographs on the Elevation of Carcinogenic Risk
     of Cheaicals to Man.  Vol. 9s  Some JUiridines, N-, 5- ,
     and 0-Mustards and Selenium.  World Health Organization,
     Lyon, France.  Pp. 117-123

NATIONAL INSTITUTE FOR OCCUPATIONAL SAFETY AND HEALTH (NIOSH) .
     1984.  Registry of Toxic Effects of Chemical Substances
     Data Base.  Washington, D.C.  April 1984

SAX, N.I.  1975.  Dangerous Properties of Industrial Materials.
     4th ed.  Van Nostrand Reinhold Co., lew York.  1,258 pages


bi§(2-Chloroethyl) ether
Page 3
October 1985


                               13"*

-------
 O.S.  ENVIRONMENTAL  PROTECTION AGENCY  (OSEPA).  1979.  Water-
      Related Environmental rate, of 129 Priority Pollutant*.
      Washington, D.C.  December 1979.  1»A 440/4-79-029

 U.S.  ENVIRONMENTAL  PROTECTION AGENCY  (D3EPA).  1980-  Aabitnt
      Water Quality  Criteria  for Chloroalkyl  Ether*.  Offict
      of Water Regulations and Standard*, Criteria and Standards
      Division!.  Washington, D.C.  October 1980.  EPA 440/5-90-030

 O.S.  ENVIRONMENTAL  PROTECTION AGENCY  (OSEPA).  1985.  H«alth
      Assassatnt Doeuaant for Diebloroai*than* (M«thyltn« Chloridt).
      Offie* of Health and Environmental Assessment.  Washington,
      D.C.  February 1985.  EPA 600/8-82/004F

 WEAST, R.E. ed.  1981.  Handbook of Chemistry and Physics.
      62nd ed.  CRC  Press, Cleveland, Ohio.   2332 pages
bis(2-Chloroethyl)ether
Page 4
October 1985
                                                                   J

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                            CHLOROFORM
Summary
     Chloroform  (trichloromethane) Is often produced during
the chlorination of drinking water and thus is • common drinking
water contaminant.  It is volatilt in surface waters and is
not likely to be persistent in the environment.  Chloroform
caused an increase in kidney epithelial tumors in fats and
in hepatocellular carcinoaas in mice.  In addition, there is
suggestive evidence from epidemiological studies that exposure
to chloroform and other trihalomethanes is associated with
an increased incidence of bladder tumors in humans.  Other
toxic effects of chloroform include central nervous system
depression; eye, skin, and gastrointestinal irritation; and
damage to the liver* heart* and kidney.
CAS Humber:  67-66-3

Chemical Formula:  CHC1-

IUPAC Namei  Trichloromethane


Cheroical and Phyaical Properties

Molecular Weight:  119.38

Boiling Point:  61.?*C

Melting Point:  -63.5*C

Specific Gravity:  1.4832 at 2Q»C

Solubility in Water:  8,200 mg/liter it 20*C

Solubility in Organics:  Soluble in acetone; miscible with
                         alcohol* ether, bensene, and ligroin

Log Octanol/Water Partition Coefficient!  1.9?

Vapor Pressure:  150.5 mm Hg at 20*C

Vapor Density:  4.12
Chloroform
Page 1
October 19S5

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 Transport  andfate

      Volatilization  into  the  atmosphere  is  the major  transport
 proceaa  foe 'removal  of  chloroform  from aquatic systems  (U5SPA
 1979).   One*  in  the  tropoapbere, chloroform ia attacked  by
 bydroxyl radicala with  tht  subsequent formation ol phosgene
 (CXI,)  and poaaibly chlorine oxide  (CIO) radicala.   Weither
 of  these rtaction products  ia likely to  persist} phosgene ia
 readily  hydrolyzed to hydrochloric acid  and carbon dioxide.
 Reaction with  hydroxy radicala ia  thought to b« the primary
 environmental  fata of chloroform.  However, chloroform that
 remains  in the tropoaphere  may rtturn to aarth in prtcipitation
 or  adsorbed on partieulates,  and a avail amount may diffuse
 upward to  the  stratosphere  whart it  photodiaaociataa  via inter-
 action with ultraviolet light.

      Photolysis, hydrolysis,  and aorption do not appear  to
 ba  significant environmental  fata  procaaaaa for chloroform.
 However, aorption procaaaaa may hava aoma importance  aa  a removal
 machani SB  in groundwater  and  soil.   Tha  log octanol/water parti-
 tion  coefficient indicataa  that this compound may bioaccumulate
 under conditions of  constant  exposure.   Studiaa with  matin*
 organisms  provide evidence  for only  weak to moderate  bioaccunu-
 lation.  Although chloroform  is aomewhat lipopbilic and  tenda
 to  b* found at higher concentrationa in  fatty tiaauaa/ there
 ia  no evidence for biomagnification  in aquatic food chains.


 Health Effects

     Chronic administration of chloroform by gavaga is reported
 to  product a doaa-ralatad incraaa* in the) incidanca of kidney
 epithelial tumors in. rats and a doaa-ralatad increaaa in the
 incidence  of hepatocellular carcinomas in mica (IARC  1979,
 OSZPA 1980).   Epidamiological studies suggest that higher con-
 centrations of chloroform and other  trihalomethanes in water
 aupplies may be associated  with an increased frequency of bladder
 cancer in  huaana.  However, these  results ace not sufficient
 to  establish cauaality.   An increased incidence of fetal abnor-
malities MIS reported in  offspring of pregnant rats exposed
 to  chloroform  by inhalation.   Oral doses of chloroform that
 caused maternal toxicity  produced  relatively mild fetal  toxicity
 in  the form of reduced  birth  weights.  There are limited data
 suggesting that chloroform  lias mutagenic activity ia  some test
 systems.   However, negative results  have been reported for
 bacterial  mutageneais assays*

     Huaana may be exposed  to chloroform by inhalation,  inges-
tion, or skin  contact.  Toxic effects include local irritation
of  the skin or eyes*  central  nervous system depression*  gastro-
 intestinal irritation,  liver  and kidney  damage, cardiac  arrhyth-
mia, ventricular tachycardia, and  bradycardia.  Death from
Chloroform

October 1983
                                                                   J

-------
chloroform overdosing can occur and is attributed to ventricular
fibrillation.  Chloroform «n*sth*sia can produce delayed death
as a remit of liver, necrosis.

     Exposure to chloroform by inhalation, intragastric ad-
ministration, or intraper itoneal injection produces liver and
kidney damage in laboratory animals.  The oral LD,Q and inha-
lation LCTnvalues for the rat are 908 mg/kg and 3f,QQO mg/m3
per 4 hours, respectively (ACGIH 1980) .


Toxicity to Wildlife and Domestic Animals

     Limited information Is available concerning the toxicity
of chloroform to organisms exposed at known concentrations
(DSEPA 1980).  Median effect concentrations for tvo freshwater
and one invertebrate species range Iron 28,900 to 115,000 pg/liter.
Twenty-seven day LCSO values of 2,030 and 1,240 pg/liter were
reported for embryo-larval tests with rainbow trout in water
at two levels of hardness.  The only reliable result concerning
the toxicity of chloroform to saltwater aquatic life is a 96-hour
LCSO value of 81,500 yg/liter for pink shrimp.

     An equilibrium bioconcentration factor of six with, a tissue
half-life of less than 1 day was determined for the bluegill.
Although chloroform is not strongly bioaccunulated, it. is thought
to be widely distributed in the environment and can be detected
in fish, water birds, marine mammals, and various crops.


Regulations and Standards

Aabient Water Quality Criteria (DSEPA) »

     Aauatic Life

     The available data are not adequate for establishing criteria,

     Human Health

     Estimates of the carcinogenic risks associated with lifetime
     exposure to various concentrations of chloroform  in water
     arei

                                 Concentration

                                 1.90 tig/liter
                                 0.19 Mf /liter
                                 0.019
GAG On it Risk  (USEPA) i  «.lxlO~2(«gAg/day»~l
Chloroform
Page 3
October 1985

-------
 Primary  Drinking Water  Standard:   0.10 mg/littr  (total  trihalo-
 methanes)

 HIOSH  Recommended Standard i  0.8 mg/m3 1-hr Ceiling level

 OSHA standard!  244 «g/m3 Calling  Level

 ACG1H  Threshold Lilit Valuei   SO mg/«3 (suspected buaan
                               carcinogen)


 REFERENCES

 AMERICAN CONFERENCE Of  GOVERNMENTAL  INDUSTRIAL HYGIENISTS  (ACGIH).
     1980.  Documentation of the Thrathold Liait Values.   4th
     td.  Cincinnati* Ohio.  48S pages

 INTERNATIONAL AGENCY FOR RESEARCH  OR CANCER  (IARC) .  1979.
     IARC Monograph* on the Evaluation ol Carcinoganic Risk
     of  Chamicala to Huaant.   Vol. 20i  Some Haloganatad Hydro-
     carbons.  World ••alts Organization, Lyon, Franca.  Pp. 408-415

 NATIONAL INSTITUTE FOR  OCCUPATIONAL  SAFETY AMD HEALTH  (NIOSH) .
     1983.  Ragiitry of Toxic  Iffactc of C&oieal Subttanca*.
     Data Bas*.  Washington* D.C.  Octobar 1983

 SAX, N.I.   1973.  Dangarous Propartias of Induatrial Materials.
     4th ad.  Van Hostrand Rainhold  Co., Haw Torlc

 0.S. ENVIRONMENTAL PROTECTIDH  AG2NCY (USEPA).  1979.  Watar-
     Ralatad Environaantal Fata of 129 Priority Pollutants.
     Washington, D.C.   Daea*bar 1979.  EPA 440/4-79*029

 U.S. ENVIRONMENTAL PROTECTION  AGENCY (OSEPA).  1980.  Ambient
     watar  Quality Critaria foe Chloroform.  Office of w«ter
     Regulations and Standards, Critaria and Standards Division,
     Washington, B.C.   October 1980.  EPA 440/5-80-033

 O.S. ENVIRONMENTAL PROTECTION  AGZNCY (D3EPA).  1984.  Health
     Effect! Asseisaent foe Chloroform.  Environmental Criteria
     and Assessment Office* Cincinnati* Oblo.  September 1984.
     ECAO-CIN-H010  (Final Draft)
U.S. ZNV1ROHMZHTAL PROTBCTIOH AGWCY  (USEPA).  1985.  Health
     Assessment Document for Chloroform.  Office of Health
     and Environmental Assessment, Washington, D.C.  September
     1985.  IfA 600/8-84/004F

WEAST, R.S.* ed.  I9il.  Handbook of  Chemistry and Physics.
     62nd ed.  CRC Press, Cleveland,  Ohio.  2332 pages
Chloroform
Page 4
October 1985
                                                                   J

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                        p~CHLORO-m-CR£SOt
 Summary
     p-Chloro-m-cresol  is moderately soluble in water and is
 readily, degraded during  aerobic sewage treatment.  However, it
 is*probably moderately persistent in the natural environment.
 p-Chloro-m-eresol  causes dermatitis and natural allergic reac-
 tions  in sensitive individuals.  It causes kidney damage in
 nice.   p-Chloro-m-cresol was acutely toxic to Cathead minnows
 at concentrations  of  30  ug/litpr.
CAS Humbert  59-50-7

Chemical Foraulai  c-H-CH-ClOH

IUPAC Hants  4-Chloro-a-cresol

Important Synonyms and Trade Harness  4-Chloro-3-methylphenol,
                                     3-chloro-S-hydroxytoluene,
                                     3-methyl-4-chlorophenol

Chemical andPhysicalProperties

Molecular Weights  142.59

Soiling Points  253*C

Melting Points  66-68»C

Specific Gravity:  1.213 at 1S*C

Solubility in Waters  3,850 ng/liter

Solubility in Organicsi  Soluble in alcohol and ether

Log OctanolAbater Partition Coefficient!  2.95 (calculated)


Transport and Pate

     Experimental evidence with related compounds and theoretical
consideration* suggest that intramolecular photolysis is the
most likely environmental fate for p-chloro-m-cresol.  These
reaction* could produce a aixtur* of compounds from initial
intermediates in which the methyl group becomes chlorinated
or becomes oxidised to a bensyl hydroperoxide.  Although little
information concerning other environmental processes is avail-


p-Chloro-m-cresol
Page 1
October 1985

-------
 able,  it  appears  that  oxidation  and  hydrolysis  ar*  not  likely
 to b*  important fatas,  and  that  volatilization  and  sorption
 art not likely to b* important transport proctsaes.

     Th«  lot  octanol/vater  partition coefficient of p-chloro-
 a»cresoi  suggests that  it. aay hava a tandancy to bloaccunulate,
 but that, it  is probably not an important fata process.  Para-
 chloro-«-crasol is readily  dagcadad  during aarobic  sewage  treat-
 Bent and  is partially  dagradad by adaptad alsad cultural of
 •oil and  water aicroorganisas,   However* tha petantial  for
 bi©degradation in aabient surfaca waters or in  aoil la  unknown.
     * *        *

 Health Effects

     No information concerning tha carcinogenicity, autagenicity,
 or teratogenicity of p-chloro-m-crasol  in huaana or axparimantal
 aniaali is availabla.   iara-chloro-a-cresol* in a 1.51  aqueous
 solution, is  raportad  to produce pruritie vesicular deraatitis
 in sensitive  individuals.   Syataaic  reactions to aucous beparin
 preserved with 0.151 of an  unspecified  chlorocresol,  likely
 to be p-caloro-a-cresolr include collapse* pallor*  sweating,
 hypotension,  tachycardia* and generalised urticarial  rash.
 In another case,  severe burning  pain occurred at the  site  of
 injection with heparin  preserved with 0,151 cnlorocrasol.
 Shortly afterwards* nausea*  lightheadedneasf and drowsiness
 accompanied by pallor and sweating appeared.

     Intravenous  or subcutaneous adainistration of  p-chloro-
 n-crasol produced saver* auacla  traaors and death in  aice  and
 rats. . Damage to  ranal  tubules was also observed.   In the  mouse,
 the  reported  intravenous and subcutaneous LD,0 values are  both
 70 ag/kg.  A  subcutaneous ££.. of 400 mg/kg Ifld an  oral LD.Q
 of SOO mgAg  ara  raportad fof the rat.


 Toxicitv to Wildlife and OoaestJc Animals

     An acute tozicity  value of  30 pf/litar is reported for
 the  fathead ainnow, a fraahwater apecies.  An LC.Q value due
 to chlorosis of 95,488  uf/lltar  is reported for duckweed,  a
 freshwater plant  species.

     Mo other information concerning the tosieity of  p-chloro-
m-crasol to terrestrial wildlife and domestic aniaala is avail-
able.
p-Chloro-a-creaol
Page 2
October 1985
                                                                    '

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Regulations  and Standard!

Ambient Water Quality Criteria  (USEPA) :

     Aquatic Lift      '

     The available data, ar* not adequate for establishing criteria,

     Huaan Health

     Organoleptic criterion:  3,000 Mg/iiter


REFERENCES

NATIONAL INSTITUTE FOR OCCUPATIONAL SAFETY AND HEALTH (NlOSH) .
     1984.  Registry of Toxic Effects of Chemical Substances.
     Data. Base.  Washington, D.C.  April 19S4

SAX, H.I.  1975.  Dangerous Properties of industrial Materials.
     4th ed.  Van Nostrand Reinhold Co., New York

U.S. ENVIRONMENTAL PROTECTION AGENCY  (OSSPAK  1979.  Water-
     Related Environaental Fate of 129 Priority Pollutants.
     Washington, D.C.  December 1979.  SPA 440/4-79-029

U.S. ENVIRONMENTAL PROTECTION AGENCY  (OSEPA).  1980.  Ambient
     Water Quality Criteria for Chlorinated Phenols.  Office
     of Water Regulations and Standards, Criteria and Standards
     Division, Washington, D.C.  October 1980.  EPA 440/5-80-032

WEAST, R.E., ed.  1981.  Handbook of Chemistry and Physics.
     62nd ed.  CRC Press, Cleveland, Ohio.  2332 pages
p-Chloro-«-cresol
Page 3
October 198S
                                                Cciement AMociatM

-------

-------
                      1-CHLORO-3-WITIOB BNZIKE
 Summary
      l-Chloro-3-nitrobenzene if  used  in  tht  manufacture of
 dyts.  Tht limited information available on  tht  transport and
 fate of the chemical suggest* that biodegradation  is  an important
 fate process, but one that occurs slowly.  Consequently,  it
 is probably moderately persistent in  the environment.   1-Chloro-
 3-nitrobenzene was autagenie in  the Ames assay.  It causes
 methemoglobinemia in experimental animals and  was  reported
 to induce hemolytic activity in  rats.


 CAS Number:  121-73*3

 Chemical Formulai  CgljClNOj

 IOPAC Name:  l-Chloro-3-nitrobenzene

 Important Synonyms and Trade Names;  Chloro-m-nitrobenzen«,
      a-chloroni trobentene, ni trochlorobenzene


 Chemical and Physical Properties

 Molecular Weight:  157.56

 Boiling Pointi   23S-23€*C

 Melting Point:   46*C

 Specific Gravity:  1.534  at 20*C

 Solubility in Watert  Insoluble  in water

 Solubility in Organicsi   Soluble in alcohol, ether, and carbon
                          disulfide

 Log Octanol/Water Partition Coefficienti  2.43


 Transport and Fate

      The only information on the transport and fate of  l-chloro-3-
 nitrobeniene indicates that biodegradation by  soil bacteria
 is  an important fate process but that it occurs  slowly.  Based
 on  this data,  on information for nitrobenzene  and  ehlorobenzenes,
 and on the chemical and physical properties  of the compound,
 it  would appear that l-chloro-3-nitrobenxene is  quite persistent
 in  the environment.   Besides biodegradation, other potential


 l-Chloro-3-nitrobeniene
 Page 1
 October 1985
Preceding page blank             „.-

-------
 if  the compound  is adsorbed to huaic material n«*r  the soil
 or  water star fact.


 •ealth Efftcti

     l->Chloro-3-nitrobenzene has not bttn tested for carcinogeni-
 clty In animal bioassays.  However, both l-chloro-4-nitrobenzene
 and l-chloro-2-nitrobentene were reported to be carcinogenic
 in aice (Weisbtirger et al. 1978).  l-€hloro-3-nitrobensene
 was found to be autagenic using the Ames aaaay without metabolic
 activation in strain TA100.  no information was available on
 the teratogenieity, eabryotosiclty, or fetotosicity of l-ehloro-3-
 nitrobenzene.

     It has been reported that l-cbloro-3*nitrobenzene causes
 •athamoglobunamia in experimental animals.  It led to the for-
 mation of sulf hemoglobin in rats and was reported to have a
 heaolytie action, with resulting anemia and cyanosis.  1-Chloro-
 3-nitrobenzene is probably reduced to chloroaniline in the
 body.

     The oral LD.n in the rat is 470 *f/kf » and the mouse oral
 LD5Q Is 3 to «g/kj?


 Toiicitv to Wildlife and Domestic Animals

     No information on the tosieity of l-chloro-3-nitrob«ni«na
 to wildlife or domestic animals was available in the literature
 reviewed.


 Regulations and itandards

     No regulations or standards have been established for
 1-chlor o-3-ni trobensene .
THE MERCK INDEX.  1>7«.  ftth ad.  tlindhols, N.« ad.  Merck
     and Co., Rahway, Rev Jersey

NATIONAL MSf IfOTt FOR OCCUPATIONAL SAFETY AUD HEALTH  (NIOSH) .
     1114.  Registry of Toxic iffects of Chemical Substances.
     Data laae.  Washington, B.C.  October 1114

SAX, N.I.  1973.  Dangerous properties of Industrial Hater ials.
     4th ed.  van Noa trend Re in hold Co., Mew Tor*.  1,258 pages
1-Chloro-3-nitroben«ene
Page 2
October 1985

-------
D.S. ENVIRONMENTAL PROTECTION AGENCY {USBPA).  1179.  Water-
     Relattd Environmental Pate of 129 Priority pollutants.
     Washington, D.C.  December 1979.  EPA 440/4-79-029

VtRSCHBIRIN, K.  1977.  Handbook of Environmental Data on Organic
     Chemicals.  Van Nostrand Rainhold Co., Hew Tor*.  659 pages

IfBAST. I.E., ed.  1981.- Handbook of Chemistry and Physics.
     «2nd ed.  CRC Press, Cltv«land, Ohio.  2,332 pages

WTISBURGER, E.K.f RUSSPIELD, A.I., HAMBURGER, P., WEISBDRGER,
     J.H., BAGER, E., VAN DONGEN, C.G., and CHD, K.C.  1973.
     Testing of tventy-one environmental aromatic amines or
     derivatives for long term toxicity or carcinogenicity.
     J. Environ. Pathel. Toxicol. 2:325-356
l-Cbloro-3-ni trobeniene
Page 3
October 1915

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-------
  Summary

       Chroalua la a heavy metal that generally exists in either
  a trivalent or hexavalent oxidation state,   flexavalent chromium
  (Cr VI) is rather soluble and is quite mobile in groundwater
  and surface water.  lowever, in the presence of reducing agents
  it is rapidly converted to trivalent chromium (Cr III), which
  is strongly adsorbed to soil components and consequently is
  much'less mobile.  A number of salts of hexavalent chromium
  are carcinogenic in rate,  in addition, an increased Incidence
  of lung cancer was seen in workers occupatlonally exposed to
  chromium VI.  Hexavalent chromium also causes kidney damage
  in animals and humans.  Trivalent chromium is less toxic than
  hexavalent chromium; its main effect is contact dermatitis
  in sensitive individuals.
  CAS Number:  7440-47-3

  Chemical formulas   Cr

  IUPAC Namet  Chromium


  Chemical and Physical Propertlea (Metal?

  Atonic Weighti   51.994

  lolling Points   2«72*C

  Melting Point:   1857 + 20*C

  Specific Gravityt   7.20 at 2S*C

  Solubility la Water*  Insoluble; ICQ* compounds are soluble


  Transport and Pate

       Hexavalent Cr it quite soluble, existing in solution aa
  a component of  a complex anion*  It is not aorbed to any signifi-
  cant degree by  clays or hydrous metal oxides.  The anlonlc
  form varies according to pS and may be a chroaate, hydrochrornate,
  or dichrornate.   Because all anionic forms are so soluble, they
  ars quit* mobile la the aquatic environment.  Cr VZ Is efficiently
  Chromium
  Page 1
  October 1985
                                                             macwmm
Preceding page blank
                                  \SI

-------
 rtmoved by activated carbon and  thus  may  have  soae  affinity
 for organic aaterials In natural wattr.   Cr VI la a moderately
 strong oxidizing aftnt and reacts with  reducing Materials  to
 Cora trlvalenfc ehroaium.  Most Cr XII in  the aquatic environment
 Is hydrolyied and precipitates as chromiun hydroxide. Sorption
 to sediments and bioaccuaulation will remove much of the remain-
 ing Cr III froa solution*   Cr III.is  adsorbed  only  weakly  to
 inorganic Materials.  Cr III and Cr VI art readily  interconver-
 tible in nature depending on aicroenvlronaentai conditions
 such .as pH,  hardness, and the types of other compounds present.
 Soluble fonts of chroaiua accumulate  if aabient conditions
 favor  Cr VI.- Conditions favorable for conversion to Cr III
 lead to precipitation and adsorption  of chromium in sediments.

      In airi  chromium is associated alaost entirely with particu-
 late matter.   Sources of chromium in  air  include windblown
 soil and particulate emissions froa industrial processes.
 Little Information Is available  concerning the relative amount3
 of Cr  III and Cr VI  in various aerosols.  Relatively small
 particles can fora stable aerosols and can be  transported  many
 miles  before  settling out.

      Cr III  tends to be adsorbed strongly onto clay particles
 and organic  particulate matter,  but can be mobilized if it
 is completed  with organic molecules,  Cr  III present in minerals
 is mobilized  to different  extents depending on the  weatherability
 and solubility of the mineral in which  it is contained,  aeia-
 valent compounds are not strongly adsorbed by  soil  components
 and Cr VI is  nobile  la groundwater.   Cr VI is  quickly reduced
 to CR  III in  poorly  drained soils having  a high content of
 organic matter.   Cr  VI of  natural origin  is rarely  found in
 soils.


 Health Effects

     The hexavalent  fora of chroaiua  is* of aajor toxicological
 importance la higher organisms.   K variety of  chrornate (Cr VI}
 salts  are carcinogenic In  rats and an excess of lung cancer
 has been observed aaong workers  la the chroaate-producing  indus-
 try.   Cr VI compounds caa cause  DNA and chroasoae damage ia
 aniaals and humans,  and Cr  (VI)  trioxide  la teratogenic in the
 hanstet.   Inhalation of hexavalent chroaiua salts causes irri-
 tation and inflaamatlon of  the nasal  aucoaa, and ulceration
 and  perforation of the nasal septua.  Cr  VI also produces  kidney
 daaage  in aniaals and humans.  The liver  is also sensitive
 to the  toxic  effects of hexavalent Cr, but apparently less
 so  than the kidneys  of respiratory system.  Cr III  is less
 toxic  thaa Cr VIi  its main  effect ia  huaans is a fora of contact
 deraatitls in sensitive individuals.
Chroaiua
Page 2
October 1915

-------
Toxicitv  to Wildlife and Domestie Aniaala

     Chroaiua la an essential nutrient and Is accumulated in
a variety of aquatic and marine biota, especially benthic organ-
lias > to levelt much higher than In ambient water.  Levels
in biota, however, usually are lower than levels In the sedi-
ments.  Passage of chroaiua through the food chain can be demon-
strated.  The food chain appears to be a aore efficient pathway
for chroaiua uptake than direct uptake froa seawater.

     Water hardness, temperature, dissolved oxygen, species,
and -age of the test organisa all aodify the toxic effects of
chroaiua on aquatic life.  Cr III appears to be aore acutely
toxic to fish than Cr VI; the reverse Is true in long term
chronic exposure studies.

     Hone of the plants normally used as food or animal feed
are chromium accumulators.  Chroaiua absorbed by plants tends
to reaain priaarily in the roots and Is poorly translocated
to the leaves*  There is little tendency for chromiua to accumu-
late along food chains in the trivalent inorganic fora.  Organic
chroaiua compounds, about which little is known, can have signifi-
cantly different bioaccumulation tendencies*  Little Information
concerning the toxic effects of chroaiua on mammalian wildlife
and domestic animal species is available,


Regulations and Standards

Aabient Water Quality Criteria (USEPA):

  Cr VI i

     Aquatic Life (Proposed Criteria)

     Freshwater

          Acute toxicityt  11 uf/lU*ff
          Chronic toxicityt  7.2 pa/liter

     Saltwater

          Acute toxicityt  1,200 pg/liter
          Chronic toxicityi  54 ug/liter
                                        a*
     Hunan Health         N

     Criterion!  SO yg/liter
Chroaiua
Page 3
October 1985

-------
   Cr IXXt

      Aquatic Lift {Proposed Criteria)

      freshwater

           Acute toxicityt   . CO. t!9 [in (hardness)! +3. S€i>  Uf/Uttf

           Chronic toaicityt   ,<**«•*  [In (hardness)!) +0.537) pf/lit
-------
 NATIONAL  INSTITUTE FOR OCCUPATIONAL SAFETY AND HEALTH  (NIOSH).
      1975.  Criteria  for  • Recommended Standard—Occupational
      E*posure  to Chronion (VI).  Washington, B.C.  0BEW Publi-
      cation No.  (NIOSH) 76-129

 NATIONAL  INSTITUTE FOR OCCUPATIONAL SAFETY AND HEALTH  (NIOSH).
      1983.  Registry  of Toxic Effects of Chemical Substances.
      Data Base.  Washington, D.C.  October 1983

 NATIONAL  RESEARCH COUNCIL OF CANADA.  1976.  Effects Of Chromium
      In the Canadian  Environment.  Subcommittee on Heavy Metals
      and  Certain Other Compounds, Ottawa, Canada.  Environmental
      Secretariat Publication No. NRCC 15017

 U.S.  ENVIRONMENTAL PROTECTION AGENCY  (USEPA).  1979.  Water-
      Related Fate of  129  Priority pollutants.  Washington,
      D.C.  December 1979.  EPA 440/4-79-029

 U.S.  ENVIRONMENTAL PROTECTION AGENCY  (USEPA).  1980.  Ambient
      Water Quality Criteria for Chromium.  Office of Water
      Regulations and  Standards, Criteria and Standards Division,
      Washington, D.C. ' October 1980.  EPA 440/5-80-035

 D.S.  ENVIRONMENTAL PROTECTION AGENCY  (USEPA).  1984.  Water
      quality criterias Request for comments.  (Proposed Criteria)
      fed. Reg. 49:4551-4553

 U.S.  ENVIRONMENTAL PROTECTION AGENCY  (USEPA).  1984.  Health
      Effects Assessment for Trivalent Chromium.  Environmental
      Criteria and Assessment Office, Cincinnati, Ohio.   September
      1984.  SCAO-CIN-HO35 (Final Draft)

 U.S.  ENVIRONMENTAL PROTECTION AGENCY  (USEPA).  1984.  Health
      Effects Assessment for Bezavalent Chromium.  Environmental
      Critera and Assessment Office, Cincinnati, Ohio.  September
      1984.  ECAO-CIH-H019 (final Draft)

U.S.  ENVIRONMENTAL PROTECTION AGENCY  (UStPA).  1985.  Health
     Assessment Document  for Diehloroaethane (Methylene Chloride).
     Office of Health and Environmental Assessment.  Washington,
      D.C.  February 1915.  EPA 600/8-82/004F

WEAST, 2.1., ed.  1981.   Handbook of Chemistry and Physics.
      62nd ed.  CHC Press, Cleveland, Ohio.  2,332 pages
Chroaiua
Page 5
October 1985
                                                Cc*
                               ifS

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                             CHRYSENE
 Summary
     Chrysene  is  a  five-ringed polycyclic  aromatic  hydrocarbon
 (PAH).   It  is  rather persistent  in the environment;  biodegrada-
 tlon is  probably  the ultimate fate process.  Dermal  application
 of  chrysene produces skin  tumors in nice,  and subcutaneous
 injection produces  local sarcomas.  Chrysene was  found  to be
 auta$£Jiic using several test systeas.  Although there is little
 information on other toxic effects of chrysene, carcinogenic
 PAHS as  a group cause  skin disorders and have an  imaunosuppres-
 sive effect.
CAS Number:   218-01*9
Chemical Formulat  C^jS^
IUPAC Names   Chrysene
Important Synonyms and Trade Names*   1,2-Benzophenanthrenei
                                      bens(a)phenanthrene
Chemical and  Physical Properties
Molecular Weights  228.28
Boiling Points  44S»C
Melting Points  256»C
Specific Gravityt  1.274 at 2Q*C
Solubility in Waters  0.002 ing/liter  at  23*C
Solubility in Organicst  Soluble  in ether,  alcohol, glacial
                         and ace tie acid
Log Octanol/Water Partition Coefficient:   5.61
Vapor Pressures  10*11 to 10"* ma Hg  at  29*C
Chrysene
page 1
October 1985
  Preceding page blank

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 Transport and Fate

      V«ry little specific information  concerning  the  environ-
 mental tranaport and  fat* of  chryaene  is  available*   lowever,
 data can be derived with reasonable  confid«nc*  from information
 concerning benso(a)anthracene and other related polycyclic
 aromatic hydrocarbon* (PABs).  Dissolved  chryaene aay undergo
 rapid, direct photolysis in  aquatic  systaas.  However,  the
 relative importance of this proces*  aa an environaental fate
 ia  unknown.   Singlet  oxygen  ia the oxidant  and  quinonea are
 thai-products in photolysis reactiona involving  polycyclic aro-
 matic hydroearbona.   Free-radical oxidation of  chryaene ia
 likely to be alow and ia not  likely  to be a significant fate
 process.   Because chryaene does not  contain groups amenable
 to  hydrolysis,  this process  is not thought  to be  a significant
 environaental fate.   Volatilisation  doea  not appear to  be an
 important tranaport process.

      Chryaene probably accumulates in  the sediaent and  biota
 portiona  of  the aquatic environment, and  adsorption to  suspended
 natter is likely to be the dominant  transport process.   It is
 probable  that sorption onto sediments, soil particles,  and
 biota ia  atrongly correlated  with the  organic carbon  levels
 present.   Bioaccuaulation of  chrysene  is  expected to  be short
 term end  is  not an important  fate process*  Although  polycyclic
 aromatic  hydrocarbons with four or less aroaatic  rings, like
 chrysene,  are readily and quickly bioaccuaulated, they  also
 are  rapidly  aetabolised and excreted.  These kinds of PAHs are
 degraded  by  microbes  and readily aetabolised by aulticellular
 organisas.   Degradation by mammal• is  considered  to be  incom-
 plete;  the parent compound and metabolites  are  excreted by
 the  urinary  system.   Biodegradation  is probably the ultimate
 fate process for  chrysene.  However, the  speed  and extent of
 this process are  unknown.  Biodegradation of PAHs generally
 occurs more  rapidly in soil than ia  aquatic systems and is
 alao faster  ia  those  systems  chronically  contaminated with
 these compounds.

      Atmospheric  transport of chryiene eaa  occur, sad chrysene
 can  be  returned  to aquatic and terrestrial  systems by ataospheric
 fallout and  with  precipitation.  It  caa eater surface and ground-
 waters  by  leaching from polluted soils.


Health Bffeets

     fhe potential* for polycyclic aromatic  hydrocarbons to
 induce malignant  transformation dominates the consideration
given  to health hasards resulting from exposure.  This  is because
overt  signs  of  toxicity are often not  produced  until  the dose
Is sufficient to  produce a high tumor  incidence.
Chryseae
Page 2
October 1983
                                                                    J

-------
     HO case report* or epidealological studies on the signi-
ficance of chrysene exposure to human* are available.  However,
coal tar and other materials known to be carcinogenic to humans
say contain chrysene.  Chrysene products akin tumors In nice
following repeated dermal application.  High »ubcutan«ous doses
art reported to etsult in • low incidence of tuaor» with a
long induction time in nice.  Chrysene is coniidered to have
weak carcinogenic activity compared to benzo(a)pyrent.  Chrysene
is reported to be mutagenic in a variety of ttst tysttms.
Ho information concerning the ttratogtnic effects of ehrysene
in humans or experimental animals is available.

     Although there Is little information concerning other
toxic effects of ehrysene, it Is reported that applying the
carcinogenic PAfls to mouse skin leads to the destruction of
sebaceous glands, hyperplasia, hyperkeratosis, and ulceration.
Workers exposed to materials containing these compounds may
exhibit chronic dermatitis, hyptrktratoses, and other skin
disorders.  Although specific results with ehrysene are not
reported, it has been shown that many carcinogenic PAHs have
an imaunosupprtssive effect.


Toxicitv to Wildlife and Domestic Animals

     Adequate data for characterization of the toxicity of
chrysene to domestic animals and wildlife are not available.


Regulations and Standards

Ambient Water Quality Criteria (USE?A)i

     Aquatic Life

     The available data ar.t not adequate for establishing cri-
     teria.

     Hunan Health

     Estimates of toe carcinogenic risks associated with lifetime
     exposure to various concentrations of carcinogenic PAHa
     ia water arti

                                     Concentration
                        \.
                                     28 ng/llter
                                     2.1 ng/liter
                                     0.28 ng/liter
Chrysene
Vage 3
October 1985
                                                   Oemenc AMOCVCM

-------
AMERICAN CONFERENCE OF GOVERNMENTAL INDUSTRIAL IYGXSNISTS.
      1980.  Documentation of tha Threahold Limit Values.  4th
      ad.  Cincinnati, Ohio.  483 pages

INTERNATIONAL AGENCY FOR RESEARCH ON CANCER  (IARC).  1973.
      IARC Monograph* on tht Evaluation of Carcinogenic Risk
      of Chemicals  to Man.  Vol. 3*  Certain Polycyclic Aromatic
      Hydrocarbona  and leterocyelic Compound•.  World Htalth
      Organisation, Lyon, Franea.  Pp. 159-177

LEVIN, W. , WOOD, A.If., CHANG, I.L., YAGI, I. , MAS, H.D. , J2RINA,
      D.N., and CONWEY, A.H.  1978.  Evid«nc« for bay region
      activation of chry»»n« 1,2-dihydrodiol to an  ultimate
      carcinogen.  Cancer Res. 38:1831-1834

NATIONAL INSTITUTE FOR OCCUPATIONAL SAFETY AND HEALTH  (NIOSB).
      19S3.  Regi»try of Toxic Effect* of Cheaical  Substances.
      Data Baae.  Waibinfton, D.C.  October 1983

SAX,  N.t.  1975.  Dangeroua Properties of Industrial Materials.
      4th ed.  Van Nostrand Reinhold Co., Hew York.  1,258 pages

U.S.  ENVIRONMENTAL PROTECTION AGENCY (USEPA).  1979.  Water-
      Related Environaental Fate of 129 Priority pollutants.
      Washington, D.C.  Deceaber 1979.  EPA 440/4-79-029

0.3.  ENVIRONMENTAL PROTECTION AGENCY (DSEPA).  1980.  Ambient
      Water Quality Criteria foe Polynuclear Aromatic Hydrocar-
      bons.  Offle* of Water Regulations and Standards, Criteria
      and Standards Division, Washington, D.C*  October 1980.
      EPA 440/5-80-069
Chrysene
Page 4
October 1915

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                              COBALT
 Summary
     Cobalt generally occurs in the 0 or +2 oxidation states.
Elemental cobalt  is relatively unreactivt and is quite stable
in  air or water.  Cobalt caused injection site sarcomas in rats,
out the  results of other studies were negative} it ii not con-
sidered  to pose a carcinogenic risk to humans.  Chronic oral
exposure eauses goiter, decreased thyroid function, increased
heart and respiratory rates, and blood lipid changes.  Cobalt
causes respiratory disease among occupationally exposed workers.


CAS Number:  7440-48-4

Chemical Formula;  Co

IUPAC Name:  Cobalt


Chemical and Physical Properties (Metal)

Atomic Weight:  58.933

Boiling Point;  2,8?G*C

Melting Point:  1,49S*C

Specific Gravity;  8.9

Solubility in Waters  Insoluble; some salts as* soluble


Transport and fata

     very little cobalt appears to occur in soluble fora in
natural aquatic systems.  Several surveys show that cobalt
frequently is not detectable and that concentrations greater
than 10 Mf/litar art rare.  The »ost important control on nobility
of  cobalt in aquatic and terrestrial systeas is probably adsorp-
tion to the clay ainerals and hydrous osidas of iron, manganese,
and  aluainua that are often present in the clay fractions of
sediaents and soils.  The principal factors controlling adsorp-
tion and desorption processes ara pH, Eh, and the concentrations
of  cobalt and competing compounds.  Chelation of cobalt with
soae organic compounds can also occur.  Saall aaounts of cobalt
may  be selubilisad by bacteriological activity.  Cobalt, is
an  essential eleaent and can be accunulated by plants and animals,
though generally not to excessive concentrations.  Photolysis,
volatilization! and biotransforaation are not important environ-
mental fate processes for cobalt.  However, soae atmospheric
transport of cobalt and cobalt compounds can occur.


Cobalt
Page 1
October 1985



                              I6/

-------
     Cobalt aetal  and cobalt oxide  have  been  reported  to  cause
 injection  fit*  earcoasa  in  rats  (Gilaan  1962, |««th  I960).
 However, this type of response by itself is not generally con-
 sidered adequate evidence of a cheaical'e carcinogenic!ty.  The
 abstnct of positive carcinogenic responses in other  studies
 with experiaental  animals and the lack of epidemiologic evidence
 suggest that cobalt and  it* compound* act unlikely to  pot* a
 carcinogtnic risk  to humans.  Liaited data indicate  that  cobalt
 chloride has autagenie activity in  a variety of test systeas.
 This compound was  also reported to  cause craniofaeial  developr
 aental abnoraalities in  the offspring of mice exposed  by  intra-
 peritoneal injection during pregnancy*   No other  information
 indicating carcinogenic, mutagenic, or teratogenic activity
 is available.

     Ingestion  of  excessive amounts of cobalt as  a result of
 therapeutic administration  was reported  to produce vomiting,
 diarrhea,  and a sensation of warmth in huaans.  A lethal  dose
 of 1,500 ag/kg  was reported for a child.  Intravenous  adminis-
 tration may cause  flushing  of the face/  increased blood pressure,
 slowed respiration, giddiness* tinnitus, and deafness  due to
 nerve daaage.   Chronic oral exposure to  cobalt can cause  goiter
 and decreased thyroid function, increased heart and  respiration
 rates, and blood lipid changes.  These effects were  reported
 to occur in children receiving between 1 and € ag/kg per  day
 as part of a treatment for  aneaia.  The  syaptoas  did not  persist
 after cessation of therapy.  Cobalt salts included in  a beer
 formulation at  concentrations of 1.2 to  1.5 ag/liter were reported
 to be responsible  for a  nuaber of deaths due to congestive
 heart failure,  intake of this amount of cobalt is well below
 the amount that can noraally be ingested safely by humans.
 However, studies with experiaental  animals show that ethanol
 potentiates the toxic effects of cobalt.

     Soae  workers  oceupationally exposed to dust  during the
 manufacture and use of tungsten carbide  developed respiratory
 disease.   Cobalt metal is currently thought to be the  causative
 factor in  these eases.   Two types of disease developed!   The
 first is a nonprogressive,  asthma-like reaction that does not
 persist after cessation  of  exposure.  The second  is  "hard aetal
disease.*  This disease  is  progressive,  and after a  certain
 stage, the changes In lung  structure and function become  irre-
 versible,  with  death from cardiopulaonary insufficiency usually
occurring.

     Tn* oral L010 value" for cobalt is 1,500 ag/kg in  the rat.
The oral &0«A values for a  variety  of inorganic cobalt compounds
 range frosi loout ISO mg/kg  foe cobalt fluoride to 503  ag/kg
for cobalt acetate (Speijers et al. 1912).
Cobalt
fage 2
October 1985
                                                                 J

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 Toxicity to  Wildlife  and Domestic Animals

      Little  information regarding toxic effects of exposure to
 cobalt  or cobalt  compounds  is  available.  Acute cobalt toxicity
 is icen in Chickens at  SO ppm  in the diet  (approximately 3 mg/kg
 of body weight) per day and  in sheep at 6 mg/kg of body weight
 per day.  In sheep, daily doses of  3 mg/kg of body weight,
 which is about  1,000  times  the normal daily intake of cobalt,
 do not  produce  harmful  effects, even after several weeks.


 Regulations., and Standards

 OSHA Standard:  0.1 mg/m  TWA

 ACGIH Threshold Limit Value:   0.05  mg/m3 TWA


 REFERENCES

 AMERICAN CONFERENCE OF GOVERNMENTAL INDUSTRIAL HYGIENISTS  (ACGIH)
      1980.  Documentation of the Threshold Limit Values. " 4th
      ed.  Cincinnati, Ohio.  488 pages

 CLAYTON, G.D.,  and CLAYTON, P.B.  1980.  Patty1! Industrial
      Hygiene and  Toxicology.   Vol.  2A*  Toxicology.  3rd rev.
      ed.  John Wiley  and Sons, New  York.  2*878 pages

 GILMAN,  J.f.W.  1962.  Metal carcinogenesisi  II.  A study
      on the  carcinogenic activity of cobalt* copper, iron,
      and nickel compounds.  Cancer  Rts. 22:158-165

 HAMMOND, B.P.,  and BELILZS, R.P.  1980.  Metals.  In Doull,
      J., Klaassen, C.D., and Amdur, M.O., eds.  Casarett and
      Doull1s Toxicology:  The  Basic Science of Poisons.  2nd
      •d.  Macmillan Publishing Co.* New York.  778 pages

 HEATH,  J.C.   1960.  The histogenesis of malignant tuaors induced
      by cobalt  in the cat.  Be. J.  Cane*? 14i478-482

 NATIONAL ACADEMY  OP SCIENCES  (HAS).  1977.  Drinking Water
      and Health.  Safe Drinking Water Committee, Washington,
      D.C. 939 pages
          * *
"NATIONAL IWSTITOTI POR OCCUPATIONAL SAPETY AND HEALTH  CNIOSH).
      1984*  Registry  of Toxic  Effects of Chemical Substances.
      Data Base.   Washington, D.C.   July 1984

 SPSIJERS, G.J.A., KRAJNC, E.I., BERKVZNS, J.M., and VAN. LOGTES,
      M.J. 1982.  Acute oral toxicity of inorganic cobalt com-
      pound!  in  rats.  Pood  Chen. Toxicol. 20s311-314
Cobalt
Page  3
October  198S

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                          »*« • 6
Cobalt
Ptgt 4
October 1985


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                              COPPER
Summary
     Copper is among tht nor* mobile metals in the environment.
It is toxic to nunans at high levels? it causes irritation
following acute exposure and anemia following chronic exposure.
Sheep are very susceptible to copper toxicosis, as are aany
aquatic organisms.

Background Information

     Copper exists in a valence state of +1 or +2.  It is a
lustrous, reddish metal.  The physical properties of copper
include ductility and conductivity of heat and electricity*
Copper is found in nature as sulfide* oxide, or carbonate ore.

CAS Number:  7440-50-8

Chemical Formula:  Cu

IOFAC Name:  Copper


Chemical and Physical Properties

Atonic Weight:  €3.546

Boiling Pointi  2,567»C

Melting Point:  1»OS3*C

Specific Gravity:  8.92

Solubility in Water:  Most copper salts are insoluble, with
                      the exception of CuSO., Cu(NO,),, and
                      CuCl-  (the sore COSMOrt copper silts).
                      The fetal is insoluble in water.

Vapor Pressure*  1 mm Eg at l,e*28*C


Transport and Fate

     Copper has two oxidation states, +1  (cuprous) and +2  (cupric)
Cuprous copper is unstable in aerated water over the pH range
of most natural waters  (6 to S) and oxidises to the cupric
state.  Several processes determine the fate of copper in  the
aquatic environment!  formation of complexes, especially with
humic substances} sorption to hydrous sMtal oxides, clays,
and organic materials; and bioaccumulation.  Zn waters polluted


Copper
Page 1
October 1985

-------
 with  solublt  organic  material,  complexation  with  organic  Uganda
 can occur,  thus  favoring  th* prolonged  dispersion of  copper
 in solution.  The  presence  of organic acids  also  can  lead to
 the mobilization of copper  froa the  sediments  to  solution.
 Copper  has  a  strong affinity for  hydrous  iron  and manganese
 oxides*  clays* carbonate  minerals, and  organic matter.  Sorption
 to these Materials* both  suspended in the water colusn  and
 in the  sediment, results  in relative enrichaent of the  solid
 phase and reduction in dissolved  levels.  Sorption processes
 are quite efficient in scavenging dissolved copper and  in eon-
 trolling its  nobility in  natural  unpolluted streams.  The amounts
 of the  various copper compounds and complexes  that actually
 exist in solution  depend  on the pH, temperature,  alkalinity,
 and concentrations of other chemical species.  The levels of
 copper  able to remain in  solution are directly dependent  on
 water chemistry.   Generally, ionic copper is more soluble in
 low pi  waters and  less soluble  in high  pi waters.

      As an  essential  nutrient*  copper is accumulated  by plants
 and animalsf  although apparently  it. is  not generally  biomagni-
 fied.   Because copper is  strongly bloaccuaulated  and  because
 biogenic llgands play an  important role in complexing copper,
 biological  activity is a  major  factor in determining  the  distri-
 bution  and  occurrence of  copper in the  ecosystem.  For  example,
 bioaccumulation  patterns  may exhibit seasonal  variations  related
 to biological activity.

      Because  many  copper  compounds and  complexes  are  readily
 soluble, copper  is among  the more mobile heavy metals in  soil
 and other surface  environments.   The major process that limits
 the environmental  mobility  of copper is adsorption to organic
 matter,  clays, and other  materials.  Atmospheric  transport
 of copper compounds can also occur.


 Health  iffects

      Copper appears to increase  the mutagenic  activity  of triose
 reductone and ascorbic acid in  bacterial test  systems,  lowever,
 copper  itself does not appear to have mutagenic,  teratogenic
 or carcinogenic  effects in  animals or humans.  Dietary  levels
 of trace elements  such as molybdenum, sulfur,  tine* and iron
 can affect  the level  of copper  that produces certain deficiency
 or toxicity symptoms.  In general, more attention is given
 to the problems  associated  with copper  deficiency than  to prob-
 lems  of  excess copper in  the environment.  However, high  levels
 of copper can be toxic* to humans.

      Exposure to metallic copper  dust can cause a short-tern
 illness  similar  to metal  fume fever that is characterized by
 chiUsf  fever* aching muscles,  dryness  of mouth and throat,
 and headache.  Sxpoaure to  copper fumes can produce upper


 Copper
Page  2
October  1SSS
                                                                 y

-------
respirstory tract irritation, a aetallic or sweet  taste,  nausea,
aetal fuae fever, and soaetiaes discoloration of skin  and hair.
Individuals exposed to dusts  and aists of copper salts may
exhibit congestion of nasal mucous aeabranes, soaetiaes of
the pharynx, and occasionally ulceration with perforation of
the nasal septum.

     If sufficient concentrations of copper salts  reach the gastro-
intestinal tract, they act as irritants and can produce salivation,
nausea, vomiting, gastritis, and diarrhea.  Elimination of
ingested ionic copper by vomiting and diarrhea generally  protects
the patient froa more serious systemic toxic effects,  which
can include hemolysis, hepatic necrosis, gastrointestinal bleed-
ing, oliguria, azoteaia, heaoglobinuria, hematuria, proteinuria,
hypotension, tachycardia, convulsions, and death.  Chronic
exposure aay result in anemia.

     Copper salts act as skin irritants producing  an Itching
eczema.  Conjunctivitis or even ulceration and turbidity  of
the cornea aay result froa direct contact of ionic copper with
the eye.


Toxicity to Wildlife and Domestic Animals

     Mean acute toxicity values for a large number of  freshwater
animals range from 7,2 pg/liter for Daphni a puli ear i a  to  10,200
pg/liter for the bluegill.  Toxicity tends to decrease as hard-
ness, alkalinity, and total organic carbon increase.   Chronic
values for a variety of freshwater species range froa  3.9 pg/liter
for brook trout to 60.4 pg/liter for northern pike.  Hardness
does not appear to affect chronic toxicity.  The acute-chronic
ratios for different species range froa 3 to 1S6.  The more
sensitive species tend to have lower ratios than the less sensi-
tive species.  In addition, the ratio seeas to increase with
hardness.  Acute toxicity values foe saltwater organisms  range
froa 17 ug/liter for a calanoid copepod to $00 pg/liter for
the shore crab.  A chronic value of 54 pg/liter and an acute-
chronic ratio of 3.4 is reported for the mysid shrimp.  Long-
term exposure to 5 pg/liter is fatal to the bay scallop.

     Bioconcentration factors in freshwater species range from
zero for the bluegill to 2,000 for the alga Chlorella  regular is.
Among saltwater species, th« highest bioaccumulation factors
are those for the bivalve molluscs.  Oysters can bioaccuraulate
copper up to 28,200 tiaes without any significant  mortality.

     Sheep are very susceptible to copper toxicosis, and  pois-
oning aay be acute or chronic.  Acute poisoning is caused by
direct action of copper salts on the gastrointestinal -tract,
resulting in gastroenteritis, shock, and death.  The toxic
dose is about 200 ag/kg and is usually obtained through an


Copper
Page 3
October 108S

                                                fioementAMc

-------
accidental overdose off an antihelainthic.  Xngestion of excess
copper over a long period of tine results in absorption and
accumulation of copper by the liver.  This type of chronic
cumulative poisoning a ay suddenly develop into an acute bemolytic
crisis.  Copper intake of l.S g/day for 30 days is known to
be fatal for »any breeds of sheep.  Excessive copper may be
stored in the liver as a result of excess copper ingestion,
as a consequence of iapaired liver function* or in connection
with a deficiency or excess of other trace elements.  Sheep
eliainate accumulated copper very slowly after cessation of
exposure.

     Swine develop copper poisoning at levels of 250 ng/kg in
the diet unless sine and iron levels are increased.  Toxicosis
develops with hypochronic nicrocytic anemia, jaundice, and
marked increases in liver and serum copper levels as well as
serum aspartate afflino transferase.  High copper levels may be
found in swine because of the practice of feeding them high
copper diets ia order to increase daily weight gain.  However,
twine rapidly eliainate copper once it is removed from the
diet.  Cattle are auch aore resistant to copper in the diet
than sheep or swine.  Copper toxicity in ruminants can be coun-
teracted by including molybdenum and sulfate in the diet.


Regulations and Standards

Ambient Hater Quality Criteria (USEPA):

     Aquatic Life (Proposed)

     Freshwater

          Acute tosieityt  e<°-*05 UnChardnessU - 1.413)  M/litfr

          Chronic toiieityi  ,<••»" lin(hardness)] - 1.713) MB/lttt

     Saltwater

          Acute toxicityi  1.2 pg/liter
          Chronic toxicityi  2.0 tig/liter

     Huaan Health

     Organoleptic criterion:  1 mg/liter

National Secondary Drinking Water Standards (OSEPA):  1 ag/liter

OSHA Standardsi  1.0 ag/a* TWA (dust and mist)
                 0.1 «g/a3 TWA (fuae)
Copper
Page 4
October 1985

-------
 ACGIH  Threshold  Limit  Values:   1.0  mg/m| TWA (dusts and mists)
                                0.2  mg/rn* TWA (fume)
                                2.0  «g/mj STEL (dusts and mists
 REFERENCES
 AMERICAN  CONFERENCE  OF  GOVERNMENTAL  INDUSTRIAL HYGIENISTS (ACGIH) .
      1980.   Documentation  of  the  Threshold  Limit  Values.   4th  ed.
      Cincinnati,  Ohio.   4SS pages

 BOSTWICK, J.L.   1982,   Copper toxicosis  in  sheep.   J.  Am.  Vet.  Med,
      Assoc.  180:386-387

 NATIONAL  INSTITUTE FOR  OCCUPATIONAL  SAFETY  AND BEALTH  (NXOSH) .
      1983.   Registry of Toxie Effects of Chemical Substances.
      Data Base.   Washington,  D.C.  October  1983

 UNDERWOOD, E.J.   1979.   Trace metals in  humans and anintl  hp*ttth.
      J. Hum. Nutr. 35:37-48

 U.S.  ENVIRONMENTAL PROTECTION AGENCY (USEPA) .   1979.   Hater-
      Related Environmental Fate of 129 Priority Pollutants.
      Washington,  D.C.   December 1979.  EPA  440/4-79-029

 U.S.  ENVIRONMENTAL PROTECTION AGENCY (DSEPA) .   1980.   Ambient
      Water Quality Criteria for Copper.   Office of Water  Regula-
      tions and Standards,  Criteria and Standards  Division,
      Washington,  D.C.   October 1980.  EPA 440/5-80-036

 D.S."  ENVIRONMENTAL PROTECTION AGENCY (USEPA).   1984.   Water
      quality criteria,  Request for comments.   Fed.  Reg. 49:4551-
      4553

 U.S.  ENVIRONMENTAL PROTECTION AGENCY (DSEPA).   1984.   Health
      Effects Assessment for Copper.  Final  Draft.   Environmental
      Criteria and Assessment  Office, Cincinnati,  Ohio.   Sep-
      tember  1984.  ECAQ-CIN-H025

 WEAST, R.E., ed.  1981*  Handbook of Chemistry and  Physics.
      62nd ed.  CRC Press,  Cleveland, Ohio.   2,332  pages
Copper
Page 5
October 1985
                                                   [Clemen* A»«oci*ww

-------

-------
                              CRESOLS
 Summary
     Dermal  application  of ereaols promotes  akin tumors  in
 nice.   Crt»ol»  act  highly Irritating to the  akin, mucous mem-
 branes,  and  eyes.   They  can  impair liver and kidney function
 and  cause  central nervous systen disturbances.

 CAS  Number:   1319-77-3
 Chemical Formula:   CBjCgBjQE
 IUPAC Names   m-Cresol, o-cresol, £-cresol
 Important  Synonyms  and Trade Namest  Cresylic acid, cresylol,
                                     tricresol

 Chemical and  Physical Properties
 Molecular  Weight:   108.13
 Boiling  Point:   191-203-C
 Melting  Points   10.9-35.5»C
 Specific Gravity:   1.030-1.038 at 2S*C
 Solubility in Water:  m-Cr«aol:  23,500 mg/liter at 20'C
                      o-Cresol:  31,000 mg/liter at 40*C
                      £-Creaol:  24,000 ag/liter at 40*C
 Solubility in Organic*!  Miscible with alcohol, benzene, ether,
                         and glycerol
 Log  Octanol/Water Partition Coefficient:  2  (calculated)
Vapor Preasurej  1  ma Bg at 38-53*C
Vapor Density:   3.72
 pka:  10
Plash Point!  SO*C
Cresola
Page 1
October  1185
Preceding page blank

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 Transport  and Fate

      From  th* available  information,  it  appears  that  crtsol
 is not  very volatile  and that  the main transport process  in
 the environment  is movement  in water.  In  aerated surface waters,
 it is photooxidizedj  and it  Bay also  be  nonphotolytically oxi-
 dized by a metal-catalyzed reaction in some of these  environ-
 ments.   In addition*  biodegradation by water  and toil microor-
 ganisms is apparently an important fate  process.  Because of
 the two competing  fate processes, eresol probably is  not  very
 persistent in the  environment.


 Health  Effects

      None  of  the eresol  isomers is regarded as a carcinogenic
 initiator.  However,  it  hat  been reported  that o-, £-,  and
 m-cresol administered to mice  as 20%  solutions Tn benzene twice
 weekly  for 20 weeks promoted papillomas  initiated by  a  single
 dermal  application of 9»lQ-diaethyl-l,2-bentanthracene  (DMBA)
 (Boutwell  and Bosch 1959).   The mutagenicity  and teratogenicity
 of the  cresols have not  been adequately  assessed.

      Cresols  are highly  irritating to the  skin,  mucous  membranes,
 and eyes.   Occupational  exposure to cresols has  caused  severe
 burns and  eczema.   Although  eresol isomers have  relatively
 low vapor  pressures,  airborne  cresols have reportedly caused
 headache,  vomiting, and  digestive disorders.

      In addition to being strong irritants, cresols may impair
 kidney  and  liver functioning and cause central nervous  system
 and  cardiovascular  disturbances. The rat  oral LB.Q values
 for  o-, £-, and m-cresol ace 135 mg/kg,  180 mg/kg, and  202 mg/kg,
 respectively.  The  dermal LD-.  values for  rabbits  are 1,380 mg/kg
 and  2,050  mg/kg for the  o- ana  m- isomers  of  eresol,  respectively.


 Toxicity to Wildlife  and Domestic Animals

     Waterborne eresol isomers  are toxic to fish and  other
 forms of aquatic life.   Trout eabryos are  one of the  most sen-
 sitive  species, with  24-hour median threshold limits  (TL_)
 of  2 mg/liter  for o-cresol,  7 mg/liter for 2~cresol,  and  4 mg/liter
 for  m-cresol.  TbV~24- to 96-hour TL  for  tne bluegill  is approxi-
 mately  21.5 mg/liter  for  o-cresol anf 11.8 mg/liter for the
    isoatr.  The LDQ value"~for the alga Scenedesmus is 40  mg/liter
 for  o-  and £-  Isoaers 6ut €  mg/liter  for m-cresol.  There is
 no evidence available that the  cresols bioaccumulate  in the
 tissues of wildlife species.  No alterations  in  reproductive
 capabilities  or other  subtle changes  in  wildlife species  have
 been attributed to  these  compounds.
Cresols
Page 2
October 1985
                                                                 •J

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 Regulations  and standards

 NIOSH Recommended Standards  10 mg/m3 TWA

 OSHA Standards  (skin):  20 mg/m3

 ACGIH Threshold Limit Value:  22 mg/m3


 REFERENCES

 AMERICAN CONFERENCE OF GOVERNMENTAL INDUSTRIAL HYGIENISTS {ACGIH)
     1980.   Documentation of the Threshold Limit values.  4th
     ed.  Cincinnati, Ohio.  488 pages

 BOUTWELL, R.K., and BOSCH, D.X.  1959.  The tumor-promoting
     action  of phenol and related compounds for mouse skin.
     Cancer  Res. 19:413-424


 DOULL, J., KLAASSEN, C.D., and AMDOR, M.O., eds.  1980.  Casarett
     and Doull's Toxicology:  The Basic Science of Poisons.
     2nd ed.  Macmillan Publishing Co., Rev York.  778 pages

 LYMAN, W.J., REEHL, W.F., and ROSENBLATT, D.H.  1982.  Handbook
     of Chemical Property Estimation Methods:  Environmental
     Behavior of Organic Compounds.  McGraw-Hill Book Co.,
     New York

 THE MERCK INDEX.  1978.  9th ed.  Windholx, it., ed.  Merck
     and Co., Rahway, New Jersey

 NATIONAL INSTITUTE FOR OCCUPATIONAL SAFETY AND HEALTH {NIOSH).
     1978.   Criteria for a Recommended Standard—Occupational
     Exposure to Cresol.  Washington, D.C.  DBEW Publication
     No. (NIOSH) 78-133

 NATIONAL INSTITUTE FOR OCCUPATIONAL SAFETY AND HEALTH (NIOSH).
     1984.   Registry of Toxic Effects of Chemical Substances.
     Data Base.  Washington, D.C.  October 1984

 U.S.. ENVIRONMENTAL PROTECTION AGZNCY  (OSEPA) .  1979.  Hater-
     Related Environmental Fate of 129 priority Pollutants.
     Washington, D.C.  December 1979.  SPA 440/4-79-029

U.S. ENVIRONMENTAL PROTECTION AGENCY  (OSEPA).  1984.  Health
     Effects Assessment for Cresols.  Environmental Criteria
     and Assessment Office, Cincinnati, Ohio.  September 1984.
     ECAO-CIN-BOSO  (Final Draft)
Cresols
Page 3
October 1985

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 U.S.  ENVIRONMENTAL  PROTECTION AGENCY  (USEPA).   1985.  Health
      Assessment  Document  for Dichloromethane  (Methylene Chloride),
      Of fie*  of Health  and Environmental Assessment.  Washington,
      D.C.  February 1985.  SPA  600/8-82/004F

 \TERSCHUZREN,  X.   1977.  Handbook of Environmental Data on Organic
      Chemicals,   van Nostrand Reinhold Co., Hew York.  659 pages

      f R.B.f  ed.  1981.   Handbook of Chemistry and Physics.
      62nd  ed.  CRC  Press, Cleveland, Ohio.  2,332 pages
Cresols
Page 4
October 1985
                              /7V

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                             CYANIDE
Summary.
     Cyanide  can  be present  in many forms in  the environment;.
The  transport,  fate, and  toxicity of the chemical is quite
dependent on  the  specific fora,  Hydrogen cyanide and its simple
salts  are highly  toxic  following acute exposure by humans,
experimental  animals, and both aquatic and terrestrial wildlife.
Background Information

     Cyanide  (CM*)  is usually defined as hydrogen cyanide  (HCN)
and its salts.  The chemical/physical properties, transport
and fate, and toxicity of cyanide are quite dependent on the
fora of cyanide present.

CAS Humbert  151-50-8; 143-33-9

Chemical Pormulat  CN-

IUPAC Namei  Cyanide


Chemical and Physical Properties  '                     .  ••

Molecular Weighti  2? (BOf)

Boiling Point*  26.7*C (HCN)

Melting Points  -14*C (HCN)

Specific Gravity*  0,699 at 22*C  (HCN)

Solubility in Water»  Soluble (ECU)

Solubility in Organiect  Soluble  in alcohol and ether

Vapor Presiuret  657.3 BUB Eg at 21.S*C  (ECU)


Transport and Fate

     The transport and fate of cyanide  in the environment  is
dependent on the chemical compound containing the cyanide.
Most free cyanide will be HCN in  aquatic environments and  will
probably evaporate, although biodegradation is another possible
fate process.  Metal cyanides are generally insoluble and  for


Cyanide
Page 1
October IS8S
                                                    Clement Aeeocie

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 that  reason  will  accumulate  In  the  sediment.  Socptlon  occurs
 but  is  not considered  an  important  transport or  fat* process.
 Cyanides  move  rather freely  la  lolls but biodegradation would
 probably  significantly decrease the amount present  in the  ground-
 water.  Volatilization of iCH and nitriles may occur Iron  toil
 surfaces.  .   .


 Health  Effects

      Hydrogen cyanide  and its simple salts, such a* sodium
 cyanide,  are highly toxic by all routes.  Many reports  are
 available regarding acute poisoning in humans.  Hydrogen cyanide
 vapor is  irritating at very  low concentrations,  is considered
 dangerous at 20 ppn 120 ag/s ), and is fatal at  concentrations
 of 100  pp» (100 mg/m ) for one  hour.  HIOSH notes reports of
 chronic poisoning resulting  in  fatigue* weariness and other
 subjective symptoms in workers, but these findings have  been
 disputed by other investigators.  Chronic exposure to low levels
 off cyanid* salts has been reported-  to cause enlargement  of
 the thyroid gland in humans, apparently due to inefficient
 elimination of the cyanide metabolite thiocyanate.  NIOSH  (1976)
 concluded that there was no  evidence of carcinogenicity," muta-
 genicity, or teratogenicity  for cyanides.  Cyanide has  been
 shown to produce chromosome  breaks  in a plant, Vicia ffaba.
 Because of its mechanism of  action, inhibition of the election
 transport system  in oxidative phoaphorylation, cyanide  is acutely
 toxic to almost all forms of life.  A reduction  in.the  TLV
 for BCH froa 10 mg/m3  to a ceiling  value of 3 ag/a3 has  been
 recommended by several investigators* to prevent the various
 nonspecific effects nottd by several investigators  (ACGIH 1980}.


 Toxicity to Wildlife and Domestic Animals

      Cyanid* is acutely toxic to both freshwater and saltwater
 organisms, causing death at  levels  of about SO ug/liter  in
 sensitive species and  being  fatal to many species at levels
 above 200 ug/liter.  Final acute values were determined  to
 be 44.7 ug/llter for freshwater species and 2.03 ug/liter for
 saltwater species.  Effects  such as reduced survival and reduced
 reproduction were seen in fish  chronically exposed to free
 cyanide, concentrations of froa  10 to 50 ug/liter.  The  final
 acute chronic ratios were determined to be 10.7 and 3*5  for
 freshwater and saltwater organisms, respectively.  The  final
 chronic values were determined  by dividing the acute values
 by the  acute-chronic rati-o,  and were determined to be 4.2 foe
 freshwater species and 0.5?  for saltwater organises.  An acci-
 dental  spill of cyanide caused  the  death of 4,800 fish  In Oak
Ridge,  Tennessee.  The long-term effect* of this spill were
 not repotted.  Livestock death  and  environmental damage  were
 caused  by high levels  of cyanide leaching from a drum disposal
 site  in Illinois.

Cyanide
 Page 2
October 19SS

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Regulations and Standard!

Ambient Water Quality Criteria  (USE?A)i

     Aquatic Life  (Proposed)

     Freshwater

          Acute toxicity!  22 tig/liter
          Chronic  toxicity:  4.2 pg/lit«r

     Saltwater

          Acute toxicitys  1.0 jig/liter
          Chronic  toxicity:  0.57 pg/liter

     HunanHealth

     Criterion!  200 Mg/liter

Primary Drinking Water Standard (USEPA):  200 tig/liter

ACGIH Threshold Limit Values  5 ag/m3 TWA


REFERENCES

AMERICAN COUNCIL OF GOVERNMENTAL INDUSTRIAL HYSIENISTS (ACGIH).
     1980.  Documentation of Threshold Limit Values.  4th ed.
     Cincinnati, Ohio.  488 pages

NATIONAL INSTITUTE FOR OCCUPATIONAL SAFETY AMD HEALTH (NIOSH}.
     1976.  Criteria for a Recommended Standard—Occupational
     Exposure to Hydrogen Cyanide and Cyanide Salts (NaCN,
     KCN, andCa(CN)-).  Washington, D.C.  DHEW publication
     Ho,  (NXOSH) 77-X08

NATIONAL INSTITUTE FOR OCCUPATIONAL SAFETY AND HEALTH (NIOSH}.
     1983.  Registry of Toxic Effects of Chemical Substances.
     Sata Hase.  Washington, D.C.  October 1983

U.S. ENVIRONMENTAL PROTECTION AGENCY  (USEPA).  1979.  Water-
     Related Environmental Fate of 129 Priority Pollutants
     Washington, D.C.  December 1979.  SPA 440/4-79-029

U.S. ENVIRONMENTAL PROTECTION AGENCY  (USEPA).  1980.  Ambient
     Water Quality Criteria for Cyanides.  Office of Water
     Regulations and Standards, Criteria and Standards Division,
     Washington, D.C. 'October 1980.  EPA 440/5-80-037
Cyanide
Page 3
October 1985

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U.S. ENVIRONMENTAL PROTECTION AGENCY  (USEPA) .  1983.  Revised
     Section B of Ambient Water Criteria for Cyanide—Aquatic
     Toxicology.  Draft Report.  Office of Water Regulations
     and Standard!» Criteria and Standards Division, Washington,
     O.C.  August 1983

U.S. ENVIRONMENTAL PROTECTION AGENCY  (DSEPA).  1984.  Health
     Effects Assessment for Cyanide*  Environmental Criteria
     and Assessaent Office, Cincinnati, Ohio.   September 1984.
     1CAO-CIN-B011  {Final DraftJ

VERSCHUEREN, K.  1977.  Handbook of Environmental Data on Organic
     Chemicals.  Van Nostrand Reinhold Co., Mew York.  659 pages

WEAST, R.E., ed.  1981.  Handbook of Chemistry and Physics.
     62nd ed.  CSC Press, Cleveland, Ohio.  2,332 pages
Cyanide
Page 4
October 1985
                                                                J

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                          CYANURIC ACID
 Summary
     Cyanuric  acid  has  baen  used  as  a  selective herbicide,
 Thtrt  is  limited  evidence  that  it Bay  cause tumors  in mice
 and  rats.  Chronic  exposure  to  high  doses can causa  kidney
 damage.


 CAS  Number:  108-80-5

 Chaaical formula:   C3a3HjO|

 IUPAC  Haaet  Cyanuric acid

 Important Synonyms  and  Trade Names:  Isocyanuric acid; sya-triazine-
                                     triol; l,3,5-triazine-2,4,6
                                     (lH,3H,5H)-trion«; 2,4,6-tri-
                                     hydroxy-l,3,5-triazine; trieyani
                                     acid} trihydroxycyanidine


 Chemical and Physical Properties

 Molecular Weight:   129.08

 Soiling Pointi  Oecompoaea

 Malting foints  Higher  than  360*C (decomposes)

 Specific Gravityt   2.5  at 20*C

 Solubility in Wateri  2.S to S  g/liter

 Solubility in Organic*i  Inaoluble in cold Bethanol, ether, acetone,
                         benzene, chloroforaj soluble in not alcohols


 Transport and fata

     Cyanuric acid  axiata priaarily  in two equilibrating tauto?
 aerie  apaciaat  a triozo fora and •  trihydroxy fora.  The trioxo
 form ia thought to  predominate  in the crystalline fora of this
 compound and in solution.  The  trihydroxy fora pradoainatas
 in baaic solution,  very little information concerning environ-
mental transport and fata  is available.  In general, cyanuric
 acid ia chemically  stable and relatively inart.  Volatilization
 and atmospheric transport are not likely to ba significant
 environmental processes.  Based on its low solubility in organic
 solvents, aorption  to organic particulatas and bioaccuaulation


Cyanuric acid
Page 1
October 1985

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probably do not occur to any significant extent.  When adminis-
tered to experimental animals at high doses, siost of the compound
is excreted unchanged.  Soae biodegradation has been reported
to occur, and it Bay be the predominant fate process for cyanuric
acid.


Health Effects

     Cyanuric acid exhibited a lov tumorigenie potential in
one study with rats and nice exposed by subcutaneous, oral,
and dermal routes.  Tumors appeared after latent periods of
more than IS months.  The study was conducted without concurrent
controls, and the result* must bet considered equivocal.  No
mutagenic, teratogenic, or reproductive effects resulting from
exposure to cyanuric acid have been reported.  In general,
eyanurie acid appears to have a low degree of toxicity.  Chronic
exposure at high doses ha* produced kidney changes.  The oral
LD5Q value for the rat is 500 ng/kg.


Toxicity to Wildlife and Domestic Animals

     Adequate data to characterize the toxicity to wildlife
and domestic animals are not available.
REFERENCES

CLAYTON, G.D., and CLAYTON, F.E., eda.  1981.  Patty*s Indus-
     trial Hygiene and Toxicology.  Vol. 2At  Toxicology.
     John Wiley and Sons, New York.  Pp. 2715-2769

KIRK-OTHMER ENCYCLOPEDIA OF CHEMICAL TECHNOLOGY.  1979.  Vol. 7:
     Cyanuric and Isocyanuric Acids.  3rd ed.  John Wiley and
     Sons, New York.  Pp. 397*410

THE MERCK INDEX.  1976.  9th ed.  Windholz, M., ed.  Merck
     and Co.f Rahway, New Jersey

NATIONAL INSTITUTE FOR OCCUPATIONAL SAFETY AND HEALTH  (NIOSH).
     1984.  Registry of Toxic Effects of Chemical Substances.
     Data Base.  Washington, D.C.  October 1984

SAX, N.X.  1975.  Dangerous Properties of Industrial Materials.
     4th ed.  Van Nostrtfnd Reinhold Co., New York.  1,258 pages
Cyanuric acid
Page 2
October 1985
                                                                   I

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                               UUi
Summary

     DOT i» an organochlorine pesticide, which together with
its metabolites, i* very persistent in th* environment.  DDT,
DDE, and ODD have been shown to be carcinogenic in mice.  They
primarily cause liver tumors, but they also increase the inci-
dence of lung tumors and lymphomas. . in addition, DDT is a
reproductive toxin.  Chronic exposure can damage the central
nervous system and liver.  DDT and other organochlorlne pesti-
cides.-are highly toxic to aquatic organisms and are responsible
for the decreased reproductive success of aany bird species.
Background Information

     Technical DDT is a Mixture containing 65-80% p,p'-DDT, 15*
20% o,p'-DDT, up to 41 p,p'-DDD, and traces of other materials.
Metabolites of DDT include p»p»-001 and o,p'-DDD.  The DDT
isomers and metabolites are usually found together and generally
have similar properties; therefore, they will be considered
together.  Where differences occur the specific isomer will
be identified.  DDT will, be used to refer to the combination
of technical material and metabolites.  Specific DDT isomers
will be identified at such.
CAS Numberi
p,p'-DDTi  50-29-3
e,p«-DDTt 78i-Q2-«
p,p«-DODi  72-S4-S
0,p'-DDDi  53-19-0
p,p'-DDEi  72-55-9
Chemical Formulat
      p«p*- and o,p'*DDTi
      p,p'- and o,p'-DDDi
      p,p** and o,p'-DDEi
                                        cl€i§ci4
TUPAC Namei
p,p'-DDTt  l,l,l-Trichloro-2,2-bis(4-chloroph«nyl)
           ethane
o,p'-DDTi  l»l,l-Ttichioro-2-{2-chlorophenyl)-2-
        -  C4-chlorophenyl)ethane
p,p'-DDDi  l»l-Dichloro-2f2-bisC4-chlorophenyl)-
           ethane
o,p'-DDEt  l,l-Dichloro-2,2-bis{4-chloropbenyl)-
           ethene
DDT
Page I
October 1985
                        Iff

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 Important  Synonyns  and  Trads  ftaaast

           DDTt   Dichlorodiphenyltrichloroathana,  dicophans,
                 chlorophanothana* Gasarolf  Raocid
                 TOIf  Rot liana
 Chaaical  and Physical  Propartias

 Molacular If light:   o»p»- and p,p'-DDT»   354.3
 '   ,         -        .             ODD i   320
                                   ODli   311
Boiling poinfct

Melting Point t
                 DDTi   2«0*C
DDTi
OOOs
DOlt
                       109«C
                       112*C
                        93 «C
 Solubility  in v«t«rt  p,p'-DDTt   5.5  M9/littr
                      0,p'-DDTl   2i
                      p,p'-DDDi   20
                           DDBi   14 H9/lit«r

 Solubility  in Organic* t  DDTi  Solubl*  in act ton* , b«ni«n*»
                               eyclob* xanana f »orpholin«f pyri-
                               dinar  and diozana

 Log Oct»nol/W*tar Partition Coaffieianti

          DOTs  4.9S
     p.p'-DDTi  3.98
     i V-DDDt  S.99
     o,p*-DOOs  6. OS
          DDEs  S.C9
Vapor Praaaurai
                            Hg at 2S«C
                            19 at 30»C
                            Bf at 30*C
                            Hg at 30 *C
                            Hg at 30 *C
                            Eg at 20*C
Transport and Fata

     DDT and its »*tabolita« ara vary p*rai*tant in th« environ-
•ant.  Volatilisation is probably tha aoat important transport
procaaa Iron soil and trattr for p,p*-DDT and ofp'-DDTr as avi-
danead by tha ubiquitous natura of 007 in tba anvironsant.
DOT
P»g« 2
Octobar 19tS

-------
jorption  and  bioaccumulation  are th« most important transport
processes for the  DOT isomers.   Although It only occurs slowly,
the  ultimate  Cite  process  for p,p'-DDT,  o,p'-DOT, and ODD is
biotransfornation  to fora  bis(2-chlorophenyl)methanone (ODCO).
Indirect  photolysis  nay  also  be important for  p,p*-ODT and
o,p'-DDT  in aquatic  environments.   For DDE,  direct, photolysis
•is the  moat important ultimate  fate process in the environment,
although  biotransformation nay  also be important.


Hearth  Effects

     DDT,  ODE,  and ODD have been shown to be carcinogenic to
nice, primarily causing  liver tumors, but also causing lung
tumors  and lymphomas.  DDT does not appear to  be autagenic,
but  it  has caused  chromosomal damage.  There is no evidence
that DDT  is a teratogeni but  it is  a reproductive toxin,  causing
reduced fertility, reduced growth of offspring, and fetal mor-
tality.

     Chronic  exposure to DDT  causes a number of adverse effects,
especially to the  liver and central nervous system (CMS).  DDT
induces various microsoraal enzymes  and therefore probably affects
the  metabolism  of .steroid  hormones  and exogenous chemicals.
Other effects on the liver include  hypertrophy of the parenchymal
cells and  increased  fat deposition,  in  the CMS, exposure to
DDT  causes behavioral effects such  as decreased aggression
and  decreased conditional  reflexes.  Acute exposure to large
doses or  chronic exposure  to  lower  doses causes seizures.
The  oral  LD5Q is between 113  and 450 mg/kg for the rat and
is generally  higher  for other animals.

     DDT,  ODD,  and DDE are bioconcentrated and stored In  the
adipose tissues of most animals.


Toxicitv  to Wildlife and Domestic Animals

     DDT  has  been  extensively studied in freshwater inverte-
brates  and fishes  and is quite  toxic to  most species.  The range
of toxicities .was  0.18 to  1,800 jig/liter and the freshwater
final acute value-  foe DDT  and its isomers was  determined  by
EPA  to  b*  1.1 ug/lit*f«  Saltwater  species were somewhat  more
sensitive  to  DDTj  the saltwater final acute value for the DDT
isomers was 0.13 ng/liter. Only one chronic toxlcity test
on aquatic species was reported. This test indicated that
the  acute-chronic  ratio for DDT might be high  (65 in the  reported
study), but the,data were  insufficient to allow calculation
of a final acute-chronic ratio.  DDT, ODD, and DDE are biocon-
centrated  by  a  factor of 10  to 10  .
DDT
Page 3
October 1985

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      DOT,  ODD,  DDE and tht  other  persistent  organochlorine
 pesticides art  primarily responsible  for  the great  decrease
 in the reproductive capabilities  and  consequently in  the popu-
 lations of fish-eating birds,  auch  aa the bald eagle,  brown
 pelican, and osptey.  DDT haa  alao  been ahown to decrease th*
 population* of  nuaerous other  speeiea of  waterbird*,  raptors,
 and passerines  significantly.


 Regulations and Standards

 Aabitnt Water Quality Criteria (DSEPA)t

     'Aquatic Life

 DDT:  Freshwater

           Acute toilcityi   1.1 py/liter
           Chronic  toxicityi  0.001  |ig/liter

      Saltwater

           Acute toiicityi   0.13
           Chronic  toiicityi  0.001

 DDD and DDEi  the available  data are not adequate for establishing
              criteria.   However,  EPA  did  report the lowest
              values known to be toxic la  aquatic organises.

      Freshwater

         Acute  toxieltys  DDDi  O.f ug/lite*
                          DDIt  10SO  uf /liter
         Chronic toiicityj  DDD i DDEs  lo available data

      Saltwater

         Acute  toxicitvi  DDDi  3.1 uf/iitec
                          DOBi  14  Mff/liter
         Chronic toxieitys  DDD i DDIt  Ho available data

     luaan Health

      Estimates  of  the  carcinogenic  risk!  associated with lifetiae
      exposure to various concentrations of DDT in water arts

         lisfc             v         Concentration

         10~f                      0.24 ng/liter
         10*1                      0.024 ng/liter
         10 *                      0.0024 ng/liter
DDT
Page 4
October ISiS
                                                                   j

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CAG Unit Risk  (USEPA)t  0.34  (agAg/day)'1

OSHA Standard  (air):  1 ag/m3 TWA

ACGIH Threshold Llait Value:  1 mg/m3 TWA  w -   	"


REFERENCES

AMERICAS CONFERENCE OP GOVERNMENTAL INDUSTRIAL HYGIENISTS (ACGIH).
     1980.  Documentation of the Threshold Limit Values.  4th
     •d.  Cincinnati, Ohio.  488 pages

AMERICAN CONFERENCE OF GOVERNMENTAL INDUSTRIAL HYGIENISTS (ACGIH).
     1980.  Documentation o£ the Threshold Limit Values.  4th
     ed.  Cincinnati, Ohio.  488 pages

EXECUTIVE OFFICE OF THE PRESIDENT.  1971.  Ecological Effects
     of Pesticides on Non-Target Species.  Office of Science
     and Technology, Washington, D.C.  EOP/OST-71

NATIONAL INSTITUTE FOR OCCUPATIONAL SAFETY AND HEALTH (NIOSH).
     1983.  Registry of Toxic Effects of Chemical Substances.
     Data Bast.  Washington, D.C.

NATIONAL INSTITUTE FOR OCCUPATIONAL SAFETY AMD HEALTH (NIOSH).
     1978.  Special Occupational Hazard Review for DDT.  Roek-
     ville, Maryland.  DEEW Publication No.  (NIOS!) 78.200

U.S. ENVIRONMENTAL PROTECTION AGENCY {USEPA).  1979.  Water-
     Related Environmental Fate of 129 priority Pollutants.
     Washington, D.C.  December 1979.  EPA 440/4-79-029

U.S. ENVIRONMENTAL PROTECTION AGENCY (USEPA).  1980.  Ambient
     Water Quality Criteria for DOT.  Office of Water Regula-
     tions and Standards, Criteria and Standards Division,
     Washington, D.C.  October 1980.  EPA 440/5-80-038

U.S. ENVIRONMENTAL PROTECTION AGENCY (USEPA).  1984.  Health
     Effscts Assessment for DDT.  Environmental Criteria and
     Assessaent Office, Cincinnati, Ohio.  September 1984.
     ECAO-CIN-H026  (Final Draft)

U.S. ENVIRONMENTAL PROTECTION AGENCY (USEPA).  1985.  Health
     Assessaent Document for Dichloromethane (Methylene Chloride).
     Office of Health and Environmental Assessaent.  Washington,
     D.C.  February 1985.  EPA 600/8-82/004F
DDT
Page 5
October 1985

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   VERSCHUEREN,  K.  1977.  Handbook of Invironaentai Data on Organ
        Chemicals.  Van Nostrand Rtinhold Co,» New York.  £59 page

   WEAST, R.i. «d.  1981.  Handbook o£ Ch«aiitry and Physics.
        62nd td.  CRC Press, Cleveland, Ohio.  2332 pages
DDT
Page 6
October 1985
                                                                 J

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                       DIBROMOCHLOROPRQPANE
Summary
     Dibromochloropropane  (DBCP) was formerly used as a soil
fumigant and nematocide.  It has been found to be carcinogenic
in nice and rats.  It causes mammary tumors (in female cats
only) and forestomach tumors when administered orally, and nasal,
tongue, and lung tumors when given by inhalation.  Men occupa-
tionally exposed to DBCP had abnormally low spera counts,  Ani-
mals studies have shown that dibromochloropropane has adverse
effects on the liver, kidneys, and blood cells.


CAS Number:  96-12-8

Chemical Formula:  C^HclrjCl

IUPAC Name;  1,2-Dibrorao-3-chloropropane

Important Synonyms and Trade Names:  DBCP, Furaazone, Seraagon


Chemical and PhysicalProperties

Molecular Weight:  236.36

aoiling Point:  196*C

Melting Point:  i»C

Specific Gravity:  2.093 at 14«C

Solubility in Water:  Slightly soluble  (probably 5-10 g/liter)

Solubility in Organica:  Miacible with oils, dichloropropane,
                         and isopropyl alcohol

Vapor Pressure:  0.8 an Ig at 21*C


Transport and Fate

     There was no information available on the transport and
fate of l,2-dibroao-3-chloropropane  (DBCP) at the time of this
review.  However, there is some information on the transport
and fate of structurally similar compounds that may be relevant
to the environmental fate of DBCP.

     1,2,3-frichloropropane was found to have a half-life of
51 minutes in stirred water, suggesting volatilization of DBCP


Dibromochloropropane
Page 1
October 1985

-------
 from water could be  significant.  However, DBCP  im  considerably
 heavier  than  1,2,3-trichloropropane  and  thus  somewhat  less
 likely to volatilize.  The  log oetanol/water  partition coeffi-
 cient, 2.28,  of 1,2-dichloropropane  suggests  that it will readily
 adsorb to organic components of soils  and sediments and, there-
 fore, be transported in dust and suspended solids.  The tendency
 of brominated aliphatics  to have higher  log octanol/water portion
 coefficients  than chlorinated aliphatics suggest D8CP  will
 adsorb to a greater degree  than 1,2-dichloropropane.   lecause
 of its water  solubility,  density, and  low vapor pressure, DBCP
 is a likely groundwater contaminant.   Its high density suggests
 that it  would settle to the bottom of  a  contaminant plume and
 ultimately to the bottom  of the aquifer.

     Based on Information of one and two carbon aliphatics,
 DBCP may be oxidized in the troposphere  by hydroxyl radicals
 and hydrolyzed in an aqueous environment.  Biodegradation of
 1,2-dichloropropane does  occur by soil microorganisms.  However,
 the amount and speed of biodegradation and chemical degradation
 of DBCP  is unknown.


 Health Effects

     DBCP has been found  to be carcinogenic in two  animal bio-
 assays and mutagenic in the Ames assay system,  in  a gavage
 study, DBCP was found to  produce significantly increased inci-
 dences of squamous-cell carcinomas of  the forestomach  of mice
 and rats and  of mammary adenocarclnomas  in female rats.  In an
 inhalation study, rats had  increased incidences of  nasal cavity
 tumors and tumors of the  tongue, while mice had increased inci-
 dences of nasal cavity tumors and lung tumors.

     Men occupationally exposed to DBCP  during its  manufacture
 were found to have abnormally low sperm  counts.  Male  rats ex-
 posed to DBCP during subchronic toxicity studies were  also found
 to have  abnormally low sperm cells as  well as degenerative changes
 In the seminiferous tubules, decreased weight of the testes, and
 an increased  proportion of  abnormal sperm cells.  Liver and kidney
 effects  have  also been noted in animal studies.  Effects range
 from dilatation of the sinusoids and centrilobular  congestion to
 cirrhosis and necrosis in the liver.   Cloudy swelling of the epi-
 thelium  of the proximal convoluted tubules and Increased amounts
 of interstitial tissue have been found in the kidneys.  Effects on
 blood cells were also noted in several studies.  These  effects
 include  severe leukoptfnias  and anemias in exposed monkeys and
 decreased activity of phagocytic cells in exposed rats.
Dibromochloropropane
Page 2
October 1985

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Toxiclty to Wildlife and Oonestie Animals

     The oral LD.fl value of DBCP to young aallards Is €6.5 rag/kg,
which  is lower tnan the oral LD_n value for the rat and mouse—173
and  25? ngAf, respectively.  Blposure to a water concentration
of 1 tag/liter DSC? for 24 hours produced a 901 aortality in
elan larv*.  At a use concentration of 20 gallons DBCP per
acre,  100% of exposed earthworms died in 1 day.  At a use rate
of 5 pounds per acre, DBCP killed 871 of the Luabricus and
231  of the Helodrilus sp. in 32 days.


Standards and Regulations

NIOSH Recommended Standard:  10 ppb  (0.1

QSHA Standard (air)s  1 ppb (i.S Mf/a3) TWA
REFERENCES

EXECUTIVE OFFICE Of THE PRESIDENT.  1971.  Ecological Effects
     of Pesticides on Nontarget Species.  Office of Science
     and Technology, Washington, B.C.  June 1971.  Pp. 30-31

TEE MERCK INDEX.  9th ed.  windholz, M., ed.  Merck and Co.,
     Rahway, Hew Jersey

NATIONAL CANCER INSTITUTE  (NCI).  1977.  Bioassay of Dibromo-
     chloropropane 'for Possible Carcinogenicity.  CAS No. 96-12-8.
     NCI Carcinogenesis Technical Report Series No. 28, Wash-
     ington, D.C.  DHEW Publication No.  (NIB) 78-828

NATIONAL INSTITUTE TOR OCCUPATIONAL SAFETY AND HEALTH  (NIOSH).
     1978.  A Recommended Standard for Occupational Exposure
     to Dibromochloropropane.  Center for Disease Control,
     NIOSH, Cincinnati, Ohio.  DHEW Publication No. (NIOSH)
     78-115

NATIONAL TOXICOLOGY PROGRAM  (NT?).  1983.  Carcinogenesis Bio-
     assay of l,2-Dibromo-3-chloropropane (CAS No. 96-12-8)
     in P344 Rats and B6C3F, Mice (Inhalation Study).  NTP
     Technical Report Series No. 206, Washington, D.C.  ORBS
     Publication No. (NIB) 82-1762

U.S. ENVIRONMENTAL PROTECTION AGENCY (OSEPA).  1979.  Water-
     Related Environmental Fate of 129 friority Pollutants.
     Washington, D.C.  Deceaber 1979.  EPA 440/4-79-029
Dibronochloropropane
Page 3
October 1985

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-------
  Summary

       Dichlorobenzene (DCB) Is probably persistent in the natural
  environment*  In rats,  chronic oral exposure to dichlorobenzene
  caused liver and kidney damage and changes in the hematopoietie
  system.  In humans, DCS is a skin and eye irritant; inhalation
  exposure causes nausea and irritates the membranes.
  CAS Number:  1,2-Dichlorobenzene (1,2-DCB) 95-50-1
               1,3-Dichlorobenzene (1,3-DCB) 541-73-1
               1,4-Dichlorobenzene (1,4-DCB) 106-46-7

  Cheaical Formulas  CgH4Cl2

  IUPAC Name:  Dichlorobenzene

  Important Synonyms and Trade Names;  Dichlorobenzene, DCB


  Chemical and Physical Properties

  Molecular Weights  147.01

  Boiling Point:  1,2-DCB: 180.5'C
                  1,3-DCB and 1,4-DCBi 173 *C

  Melting Point:  l,2-DC8i-17.Q«C
                  l,3-DCBi-24«C
                  l,4-DCBi-53»C

  Specific Gravity?  1.3 at 20-C

  Solubility In Wateri  1,2-DCBt 145 mg/liter at 25*C
                        1,3-DCBi 123 ag/liter at 25'C
                        1,4-DCB: 80 mg/liter at 25*C

  Solubility in Organics:  Soluble in alcohol, ether* acetone,
                           benzene, carbon tetrachloride, and
                           ligroin

  Log Octanol/Water Partition Coefficient:  3.38

  Vapor Pressure:  1 ma Hg^. at 20*0

  Vapor Density:  S.OS
  Dichlorobenzene
  Page 1
  October 1985
Preceding page blank

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 Henry's  Law Constants   1.99  x  10*3  atai  n3/«ole

 Flash  Points   ?1*C


 Transport  and  Pate

     Relatively little  information  concerning the envifonaental
 fate of  dichlorobenzene  (DCS)  is available.  DCB is expected
 to  volatilize  at a  relatively  rapid rate, and atmospheric trans-
 port can occur.   It has  an estimated half-life for removal fton
 agitated surface water oC 9  hours or less,  Oichlorobenzenes are
 reported to be reactive  toward hydroxyl radicals in air with a
 half-life  of about  3 days, but indirect evidence suggests that
 DCB does not hydrolyze at a  significant rate under normal envi-
 ronmental  conditions.  The high log octanol/water partition co-
 efficient  for  DCB suggests that adsorption to organic matter in
 aquatic  systems  and soil is  probably an important environmental
 fate process.   Indirect  evidence suggests that bloaccumulatlon
 may also be an important fate  process.   DCB appears to be resis-
 tant to  biodegradation.  However, it may be broken down to some
 degree by  pollutant-acclimatized microorganisms.  Sorption, bio-
 accumulation,  and volatilization with subsequent atmospheric
 oxidation  are  likely to  be competing processes, with the dominant
 fate being determined by local environmental conditions.  If
 volatilization doesn't occur,  dichlorobenzene Is probably rather
 persistent.


 Health Effects

     It  is generally thought that the available data are inade-
 quate for  assessing the  carcinogenic potential of DCB in animals
 and humans.  One case study  suggests an association between
 exposure to dichlorobenzene  and several cases of leukemia.
 DCB is reported  to  be nonmutagenic  In Salmonella typhimurlorn
 tester strains.  Mutagenic and clastogenic activity reportedly
 occurs in  soae plant test systems.  No  data are available for
 evaluating the teratogenic or  reproductive effects in animals
 or humans.

     Symptoms  of acute inhalation intoxication in humans include
 headache, nausea, and throat irritation.  DCS is also a akin
 and eye  irritant.

     A variety of other  symptoms, including weakness, fatigue,
 and anemia, have been observed after chronic dermal and inhalation
 exposure to dichlorobenzene*

     Inhalation  of DCB causes  eye and upper respiratory tract
 irritation, central nervous  system  depression, and liver and
 kidney damage  in experimental  animals.   An LC^g of approximately


Dichlorobenzene
Page 2
October  1985
                                                                    J

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4,900 »g/a3/? hours is reported for the rat.  Ho totie effects
were observed after daily 7-hour inhalation exposures of up
to 560 ag/a3 for at «ueh as ? months in several species of
experimental animals.  Hepatic porphyria is reported to occur
In rata after daily trachea! intubation of 4SS •f/aj for up
to 15 days.  Oral exposure results in stimulation of liver
•icrosomal tnzya* systems and cumulative toxicity.  The oral
LDe0 tot the rat is 500 afAg.  Chronic oral exposure to 1S8
•g7ig/day causes liver and kidney damage in rats.  Exposure
to 0.01-0.1 agAg/day products changes in the hematopoietic
system, increased prothrombin time, and altered conditioned
reflexes and enzyme activities in chronically exposed rats.
fn general, toxieity increases in the order 1,4-DCB, 1,3-DCB,
1,2-DCB.


Toxieity to Wildlife and Domestic.Animals

     The 48-hour and 16-hour LC.. values for Oaphnia and blue-
gills, respectively, tested undff static conditions, were 2,440
and 5,590 ug/liter  (1,2-DCB)f 23,100 and 5.020 ng/llter  (1,3-DCB);
and 11,000 and 4,280 ug/liter (1,4-DCB).  Two flow through
96-hour LC«n tests using fathead minnows and rainbow trout
gave values of about 3,000 gg/liter.  A freshwater chronic
value of 2,000 pg/liter is reported for the fathead minnow.
Acute values for three saltwater species ranged from 1,970 ug/liter
for the mysid shrimp to 9,SCO ug/liter for the sheepshead minnow.
No saltwater chronic values are available.  A whole body biocon-
centration factor of about 80 is reported for the bluegill.

     The 96-hour median effect levels for chlorophyll a and cell
number are 179,000 and 149,000 yg/liter, respectively, in the
freshwater alga Selenaatrum eaprieornutum.  In the saltwater
alga SXeletonema costatum the corresponding values are 44,200
and 44710U Mg/lTter, respectively.


Regulations and Standards

Ambient water Quality Criteria (USEPA):

     Aquatic Life

     The available data are not adequate for establishing criteria.

     Hunan Wealth

     Criterion:  400 ug/liter

OSHA Standard]  300 ag/m3 Ceiling Level

ACGII Threshold Limit Value:  300 «g/«3 Calling Level


Dichlorobenzene
Page 3
October 1§85

-------
REFERENCES

AMERICAN CONFERENCE Of GOVERNMENTAL INDUSTRIAL IYGIENISTS (ACGIR).
     If 10.  Documentation of the Threshold Halt valaes.  4th
     •d.  Cincinnati, Ohio.  411 pages

INTERNATIONAL AGENCY FOR RESEARCH ON CANCER (XARC1.  1912.
     XARC Monograph* on the Evaluation of the carcinogenic
     Risk of Cheaicals to Iu»«n».  vol. 29i  Sea* Industrial
     Chenlcals and Dyestuffs.  World Health Organization, Lyon
     Franc*,  Pp. 213-238

NATIONAL INSTITUTE FOR OCCUPATIONAL SAFETY AND IEALTH (NIOSff).
     1984.  Registry of Toxic Effacts of Ch««ieal Substances.-
     Data Basa.  Washington, D.C.  July 1984

SAX, N.I.  1S7S.  Dangarous Propartias of Industrial Matarials.
     4th ad.  Van Nostrani Rainhold Co.  Nav York.  1,258 pages

U.S. ENVIRONMENTAL PROTECTION AGENCY (BSEPA*.  1979.  Water-
     Ralatad Environmental Fata of 129 Priority Pollutants.
     Washington, D.C.  December 1979.  EPA 440/4-79-029

O.S. ENVIRONMENTAL PROTECTION AGENCY (DSZPA).  1980.  Aabiant
     Water Quality Criteria for Dichlorobenxenes.  Washington,
     D.C.  October 1980.  EPA 440/5-80-039

WEAST, R.E., ad.  1981.  Handbook of Cheaiftry and Physics.
     <2nd ed.  CRC Press, Cleveland, Ohio.  2332 pages
Dichlorobaniene
Page 4
October 198S

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                         ,1-DICHLOiOlTHANE
Saiwary
     1,1-Dichloroethane la quite volatile and probably is not
very persistent in aquatic environments.  Inhalation exposure
to high doses causes central nervous system depression in humans
and aay cause hepatotoxicity.  In animalsf high doses cause
liver and kidney damage and retard fetal development.


CAS Number:  75-34-3

Chemical Formula:  CH,CHC1,

IUPAC Name:  1,1-Dichloroethane

Important Synonyms and Trade Names:  Ethylidene chloride, tthylidenc
                                     dichloride


Chemical and Physical Properties

Molecular Heights  98.91

lolling feints  5?.3*C

Melting Point:  -97.0»C

Specific Gravity!  1.177C at 20«C

Solubility in Water:  5 g/liter

Solubility in Organics:  Kiscible in alcohol

Log Octanol/Water Partition Coefficient!  1.79

Vapor Pressure:  110 ma Eg at 20'C


Transport and Fate

     1,1-Diehloroethane disperses from surface water primarily
by volatilization into the troposphere, where it is subsequently
broken down by bydroxylation.  Ho studies on adsorption were
found in the literature^reviewed, bat because of its water
solubility and relatively low log octanol/water partition co-
efficient , 1,1-dichloroethane potentially could move through
soil and enter the groundwater.
1,1-Dichloroethane
Page 1
October 1985

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Health Iffeets

     Limited toxieolOfieal testing of 1,1-diehloroethane has
been conducted, although the literature indicates that 1,1-
dichloroethane is on* of th* least toxic of the chlorinated
ethanes.  An NCX bioassay on 1,1-dichloroethan* was limited
by poor survival of test aniaals of test animals, but some
marginal tuaorigenic effects were seen.  Inhalation exposure
to high doses of 1,1-dichloroethan* (over 1«,000 mg/mj) caused
retarded fetal development in rats (Schwets et al. if74J.
1,1-Diehloroethane was not found to be autagenic using the
Ames assay.  1,1-Dichloroathan* causes central nervous system
depression when inhaled at high concentrations, and evidence
suggests that the compound is hepatotoxie in humans.  Kidney
and liver damage was seen in animals exposed to high levels
of 1,1-dichloroethana.  The oral LD.A value in the rat ia
725 mg/kg.                         50


Toxicity to wildlifeand ooaeatie Animals

     No information on the toxicity of 1,1-dichloroethane to
aquatic species was reported in the literature reviewed.  Bow-
ever, the available information on th* chloro*thanes indicates
that toxieity declines with decreases in eblorlnation and that
the 1,1,1-isoaer ia less active than the 1,1,2-isoaer.  Therefore
1,1-dichloroethane is probably no more toxic than 1,2-dichloro-
ethane, which is acutely toxic at levels of 100-500 ag/liter
and has a chronic toxicity beginning at about 20 rag/liter.

     Ho information on the toxieity of 1,1-dichloroethane to
terrestrial wildlife or domestic animals was found in the sources
reviewed.


Regulations and Standards

Ambient Water Quality Criteria (OSEPA)i

     The available data war* inadequate for establiahing cri-
     teria.

OSHA Standard (air)t  400 ag/m3 THA

ACGIH Threshold Limit Value:  810 ag/a3 Tim
AMERICAN CXINPERZNCZ Of GOVERNMENTAL INDUSTRIAL HYGIZNISTS (ACGIH).
     1980.  Documentation of the Threshold Limit Values.  4th
     ed.  Cincinnati, Ohio.  488 pages


lrl*Dichloroethane
Page 2
October If85

-------
     Report from the Medical Biological Laboratory, MBL-1981-14.
     Available from NTIS, Order No. PI82-182809

RATIONAL CANCER INSTITUTE (NCI).  1917.  Bioassay of 1,1-Di-
     chloroethane for Possible Carcinogenicity.  CAS No. 75-34*3.
     NCI Carcinogenesis Technical Report Series No. 66, flashing-
     ton, D.C.  DHEW Publication No.  (NIH) 78-1316

NATIONAL INSTITUTE FOR OCCUPATIONAL SAFETY AND HEALTH  {NIOSB).
     1983.  Registry of Toxic Effects' of Chemical Substances.
     Data Base.  Washington, D.C.  October 1983

SCHWETZ, B.A., LEONG, B.K.J., and GEBRING, P.J.  1974.  Embryo-
     and fetotoxicity of inhaled carbon tetrachloride, 1,1-
     dichloroethane and methyl ethyl  ketone in rats.  Toxicol.
     Appl. Pharmacol. 28:452-464

U.S. ENVIRONMENTAL PROTECTION AGENCY  (DSEPA).  1979.  Water-
     Related Environmental Fate of 129 Priority Pollutants
     Washington, D.C.  December 1979.  EPA 440/4-79-029

U.S. ENVIRONMENTAL PROTECTION AGENCY  (USEPA).  1980.  Ambient
     Water Quality Criteria for Chlorinated Ethanes.  Office
     of Water Regulations and Standards, Criteria and standards
     Division, Washington, D.C.'  October 1980.  EPA 440/5-80-028

O.S. ENVIRONMENTAL PROTECTION AGENCY  (USEPA).  1984.  Health
     Effects Assessment for 1/1-Dichloroethane.  Environmental
     Criteria and Assessment Office, Cincinnati, Ohio.  September
     1984.  ECAO-CIN-I027  (Final Draft)

VERSCHUEREN, X.  1977.  Handbook of Environmental Data on Organic
     Chemicals.  Van Nostrand Reinhold Co., New York.  659 pages

WEAST, R.E.r ed.  1981.  Handbook of Chemistry and Physics.
     62nd ed.  CRC press, Cleveland, Ohio.  2,332 pages
1,1-Dichloroethane
Page 3
October 1985
                                                         Ammocmtmm

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                         IrZ-DlCHLOROETHANE
  Summary
       1,2-Dichloroethane  (ethylene  dichloride)  Is  a volatile
  organic  solvent,  and volatilization  and  percolation into ground-
  water  may  be  significant  routes  of transport.   It has  a low
  solubility in water and aay  be a component  in  nonaqueous-phase
  liquids.   1,2-Dichloroethane is  carcinogenic in animals and
  mutagenic  in  bacterial  test  systems;  it  is  a suspected  human
  carcinogen.
 CAS  Numbers   107-06-2

 Chemical Formulas  CHjClCHjCl

 IUPAC  Name:   1,2-Dichloroethane

 Important Synonyms and  Trade Names:   Ethylene dichloride,  glycol
                                       dichloride


 Chemical and  Physical Properties

 Molecular Weight:  98.96

 Boiling Point:   83-84*C

 Melting Points   -35.4»C

 Specific Gravity:  1.253  at 20*C
                                            ""V
 Solubility  in Water:  8 g/liter

 Solubility  in Organics:   Niscible  with  alcohol,  chloroform,
                           and ether

 Log  Octanol/Water Partition Coefficients   1.48

 Vapor  Pressure:  61 mm  If at 20*C

 Plash  Pointi  15»C (closed cup)
  1,2-Dichloroethane
  Page  1
  October  198S
Preceding page blank
                             111

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 Transport  and Fata

     The primary method of dispersion  from  surface water  for
 1,2-dichloroethane  is volatilization.  In the atmosphere, 1,2-di-
 ehloroethane is rapidly broken down  by hydroxylation, although
 some may be absorbed by atmospheric  water and return to the
 earth  by precipitation.  No  studies  on the  adsorption of  1,2-di-
 chloroethane onto soil were  reported in  the literature examined.
 However, 1,2-dichloroethane  has a low  octanol/water partition
 coefficient, is slightly soluble in  water,  and therefore leaching
 through the soil into the groundwater  is an expected route of
 dispersal.


 Health Effects

     1,2-Dichloroethane is carcinogenic  in  rats and nice, producing
 a variety of tumors.  When administered  by  gavage, it produced
 carcinomas of the forestonach and hemangiosarcomas of the circu-
 latory system in male rats;  adenocarcinomas of the mammary
 gland  in female rats; lung adenomas  in male nice} and lung
 adenomas, mammary adenocarcinomas, and endometrial tumors in
 female mice.  It is mutagenic when tested using bacterial test
 systems.  Human exposure by  inhalation to 1,2-dichloroethane
 has been shown to cause headache, dizziness, nausea, vomiting,
 abdominal pain, irritation of the mucous membranes, and liver
 and kidney dysfunction.  Dermatitis  may  be  produced by skin
 contact.  In severe cases, leukoeytosis  (an excess of white
 blood cells) say be diagnosed} and internal hemorrhaging and
 pulmonary edema leading to death may occur.  Similar effects
 are produced in experimental animals.


 Toxiclty to Wildlife and Domestic Animals

     1,2-Dichloroethane is one of the  chlorinated ethanes least
 toxic to aquatic life.  For  both fresh-  and saltwater species,
 it is acutely toxic at concentrations  greater than 118 ag/liter,
 while chronic toxicity baa been observed at 20 ag/liter.  1,2-Di-
 chloroethane is not likely to bioconcentrate, as its steady
 state bioconcentration factor was 2  and  its elimination half-
 life was less than 2 days in bluegill.

     No information on the toxicity  of 1,2-dichloroethane to
 domestic animals or terrestrial wildlife was available in the
 literature reviewed.
1,2-Dichloroethane
Page 2
October 1985
                                                                  J

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Reg u 1 at ions  and  5 ta nd a rd s
Aabient Water Quallt" Crittria  (OSEPA) :
     Aquatic Life
     The  available data, ace  not  adequate  for  establishing  critgria
     However, EPA did  report the  lowest values  known  to  be
     toxic in aquatic organisms.
     Freshwater
          Acute  toxicity:  118 lag/liter
          Chronic toxicityt   20 ag/liter
     Saltwater
          Acute  toxicity:  113 ing/liter
          Chronic toxicity;   Ho  available data
     Hunan Health
     Estimates of the carcinogenic  risks  associated with lifetime
     exposure to various concentrations of 1,2-diehloroethane
     in water are:
     Risk                         Concentration
     I0~l                         9.4  uf/littr
     10 2                         0.94 Hi/liter
     10                           0.094
CAG Unit Risk  (OSEPA) :  9.1xlQ~2  (lag/kg/day )~l
OSHA Standards:  200 mg/m| TWA
                 400 ag/Bu Ceiling Level
                 SOO mg/m  for  5 min every 3 hr, Peak Concentration
ACGXH Threshold Limit. Values.*   40 mg/o| TWA
                                60 mg/m  STEL

RgF£R£NCSS
AMERICAN CONFEBEMCE Of GOVERNMENTAL INDUSTRIAL HYGIENISTS  (ACGXH) .
     19SO.  Documentation of  the Threshold Limit Values.   4th
     ed.  Cincinnati, Ohio.   488 pages
NATIONAL INSTITUTE P01 OCCUPATIONAL SAFETY AND HEALTH  (MIOSH) .
     1976.  Criteria  for a Recommended Standard—Occupational
     Exposure  to Ethylene Dichloride  (1 ,2-Dichloroethane) .
     Washington, D.C.  DHEW Publication NO.  (NIOSH)  76-139

1,2-Dichloroe thane
Page 3
October 19 B 5

-------
NATIONAL INSTITUTE FOR OCCUPATIONAL SAFETY AMD HEALTH  (NIOSH).
     1978.  Revised Recommended Standard—Occupational Exposure
     to Ethylene Dichloride  (1,2-Dichloroethane).  Washington,
     D.C.  DHEW Publication No. (NIOSH) 78-211

NATIONAL INSTITUTE FOR OCCUPATIONAL SAFETY AND HEALTH  (NIOSH}.
     1983.  Registry of Toiic Effects of Chemical Substances.
     Data Bast.  Washington, D.C.  October 1983

0.S. ENVIRONMENTAL PROTECTION AGENCY  (USEPA).  1979.  Water-
     Related Environmental Fate of 129 Priority Pollutants.
     Washington, D.C.  December 1979.  EPA 440/4-79-029

U.S. ENVIRONMENTAL PROTECTION AGENCY  (USEPA).  1980.  Ambient
     Water Quality Criteria  for Chlorinated Ethanes.  Office
     of Water Regulations and Standards, Criteria and Standards
     Division, Washington, D.C.  October 1980.  EPA 440/5-80-029

U.S. ENVIRONMENTAL PROTECTION AGENCY  (USEPA).  1984.  Health
     Effects Assessment for  1,2-Dichloroethane.  Environmental
     Criteria and Assessment Office, Cincinnati, Ohio.   September
     1984.  ECAO-CIN-H002  (Final Draft)

U.S. ENVIRONMENTAL PROTECTION AGENCY  (USEPA)".  1985.  Health.
     Assessment Document for Chloroform.  Office of Health
     and Environmental Assessment, Washington, D.C.  September
     1985.  EPA 600/8-34/004P

WEAST, R.E., ed.  1981*  Handbook of Chemistry and Physics.
     62nd ed.  CRC Press, Cleveland, Ohio.  2,332 pages
1,2-Dichloroethane
Page 4
October 1985
                                                                J

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                       1,1-DICHUJROETHYLENE
Summary
     IjlrDiehloroethylene  (VDC, vinylidene chloride) caused
kidney tumors  (in males only) and leukemia in one study of
nice exposed by inhalation, but th« results of other studies
were equivocal or negative.  1,1-Dichloroethylene is mutagenie,
and it. caused adverse reproductive effects when administered
to rats and rabbits by inhalation.  Chronic exposure causes
liver damage, and acute exposure to high doses produces nervous
system damage.
CAS Number:  75-35-4

Chemical Formula:  CH^CCl-

IUPAC Name:  1,1-Dichloroethene

Important Synonyms and Trade Names:  Yinylidene chloride, VDC,
                                     1,1-dichloroethene, 1,1-DCS


Chemical and Physical Properties

Atomic Weight:  96.94

Boiling feints  37*C

Melting Points  -122.1«C

Specific Gravity:  1.218 at 2Q«C

Solubility in Wat«r:  400 ag/liter at 20*C

Solubility in Organic*:  Sparingly soluble in alcohol, ether,
                         acetone, benzene, and chloroform

Log Octanol/Water Partition Coefficient:  1.48

Vapor Pressures  SOO ma Hg at 20°C

Vapor Density:  3.25
                       \.

Transport and Fate

     Volatilization appears to be the primary transport process
for 1,1-dichloroethylene (VDC), and its subsequent photooxida-


1,1-Dichloroethylene
Page 1
October 1985

-------
(ion  in the ataosphere  by reaction with hydroxyl radicals  is
apparently the predominant fate process.  Inforaation on other
transport and fate mechanisms was generally lacking for 1/1-di-
chloroethylene.  However, by inference from related compounds,
hydrolysis, sorption, bioaccumulation, biotransfornation,  and
bi©degradation probably all occur but at rates too slow to
be of much significance.


Health Effects

      1,1-Dichloroethylene caused kidney tumors in aales and leu-
kemia in sales and females in one study of nice exposed by
inhalation, gave equivocal results in other inhalation studies,
and gave negative results in rats and mice following oral  ex-
posure and in hamsters  following inhalation exposure.  VDC
was autagenic in several bacterial assays.  1,1-Dichloroethylene
did not appear to be teratogenic but did cause eabryotoxicity
and fetotoxicity when administered to rats and rabbits by  in-
halation.  Chronic exposure to oral doses of VDC as low as
5 ag/kg/day caused liver changes in rats.  Acute exposure  to
high doses causes central nervous systea depression, but neuro-
toxicity has not been associated with low-level chronic exposure.
The oral LD.Q value for the rat is 1*500 mg/kg, and for tha
mouse it is 200 ag/kg.


Toxicity to Wildlife and Domestic Animals

      1,1-Dichloroethylene is not very toxic to freshwater  or
saltwater speciesr with acute LC_Q values generally ranging
from  80 to 200 mg/liter.  A chronic study in which no adverse
effects were observed indicated that the acute-chronic ratio
was less than 40; a 13-day study that produced an LC5Q of  29
ag/liter indicated that the acute-chronic ratio is greater
than 4.

     No reports of the  toxicity of 1,1-dichloroethylene to
terrestrial wildlife or domestic animals were found in the
literature reviewed.


Regulations and Standards

Aabient Water Quality Criteria  (DSEPA)i

     Aquatic Life

     The available data, are inadequate for establishing criteria,
     iowever, EPA did report the lowest values known to cause
     toxicity in aquatic organises.
1,1-Dichloroethylene
Page 2
October 1985

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     c-c«sn water
          Acute toxicity:  11,600 ug/liter
          Chronic toxieity:  Ho available data
     Saltwater

          Acute toxicity;  224,000 yg/liter
          Chronic toxicity;  No available data

     Human Health

     Estimates of the carcinogenic risks associated with lifetime
     exposure to various concentrations of 1,1-diehloroethylene
     in water are:

     Risk                        Concentration

                                 0.33 Mi/liter
                                 0.033 MS/liter
                                 0.0033 pg/liter

CAG Unit Risk (USEPA)j  1.16 (ag/kg/day)*1


REFERENCES

INTERNATIONAL AGENCY FOR RESEARCH ON CANCER (IARC).  1979.
     IARC Monographs on the Evaluation of Carcinogenic Risk
     of Chemicals to Humans.  Vol. 19:  Some Monomers, Plastics
     and Synthetic Elastomers, and Acrolein.  World Health
     Organization, Lyon, France

NATIONAL INSTITUTE FOR OCCUPATIONAL SAFETY AND lEALTH (NIOSH) .
     1983.  Registry of Toxic Effects of Chemical Substances.
     Data. Base.  Washington, D.C.  October 1983

NATIONAL TOXICOLOGY PROGRAM (NT?).  1982.  Carcinogeneais Bio-
     assay of Vinylidene Chloride (CAS No.. 75-35-4) in F344
     Rats and B6C3F, Nice  {Gavage Study).  NTP Technical Report
     Series No. 228.  Washington, D.C.  DHHS Publication NO.
     (Nil) 82-1784

U.S. ENVIRONMENTAL PROTECTION AGENCY (USEPA).   1979.  Water-
     Related Environmental Fate of 129 Priority Pollutants.
     Washington, D.C.  December 1979.  EPA 440/4-79-029

U.S. ENVIRONMENTAL PROTECTION AGENCY (USEPA).   1980.  Ambient
     Water Quality Criteria for Dichloroethylenes.  Office of
     Water Regulations and Standards, Criteria and Standards
     Division, Washington, D.C.  October 1980.  EPA 440/5-80-041
1,1-Dichloroethylene
Page 3
October 1985

-------
U.S. ENVIRONMSHmL PROTECTION AGENCY  (USEPA) .  1384.  Health
     Effects Assessment for  1,1-Dichloroethylene.  final Draft.
     Environmental Criteria  and Assessment Office, Cincinnati,
     Ohio.  September 1984.  1CAO-CIN-H051

U.S. ENVIRONMENTAL PROTECTION AGENCY  (USEPA).  1985.  Health
     Assessaent Document for Chloroform.  Office of Health
     and Environmental Assessment, Washington, D.C.  September
     1985.  EPA 600/8-84/004P

VERSCHUEREN, K.  1977.  Handbook of Environmental Data on Organic
     Chemicals.  Van Sostrand Reinhold Co., New York.  €59 pages

WEAST; U.S., ed.  1981.  Handbook of  Chemistry and Physics.
     62nd ed.  CSC Press, Cleveland,  Ohio.   2,332 pages
1i1-Dichloroethylene
Page 4
October 1985
                                                                 J

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                    1,2-trins-DICHLOROETHYLENE
Summary
     Chronic  inhalation  exposure  to 1,2-trans-dichloroethylene
 (1,2-trans-DCE)  causes liver  degeneration,  and  acute  exposure
 to  hlqh  levels  hat  adverse  effects  on  the central  nervous  system,
CAS -Slumber;   540-59-0

Chemical Formulas  CjHjCl.

IUPAC Nane:   1,2-trans-Dichloroethene

important Synonyms and Trade Names:  trans-Acetylene  dichioride,
                                     diofora


Chemical and  Physical Properties

Molecular Weight:  96.94

Soiling feint?  47. S«C

Melting Pointx  -50*C

Specific Gravity:  1.2565 at 20°C

Solubility in Water:  600 mg/Ut«r

Solubility in Organicss  Miscible with alcohol* ether, and acetone,*
                         very soluble in benzene and  chloroform

Log Octanol/Water Partition Coefficient!   1.48  (calculated)

Vapor Pressures  200 ma Hg at 14*C

Flash Pointt  3*C  (undefined iaoaeri)


T r ansport and.Fat•

     Due to the relatively high vapor pressure of 1,2-trans-
dichloroethylene (1,2-tra^is-DCE) , volatilization from aquatic
systems to the atmosphere is quite rapid and appears  to be
the primary transport process.  Aerial transport of this compound
can occur and is partly responsible foe its relatively wide
I,2-trans-Oichloroethylene
Page 1
October 1985
                                                  Ctorrwnt AMOCilCM

-------
 environmental distribution.  Although little applicable  infor-
 mation  is available, adsorption  is probably an insignificant
 environmental fate process for 1,2-trans-DCE.  The relatively
 low  log octanol/water partition  coefficient of 1,2-trans-DCE
 suggests that bioaccunulation also is a relatively insignificant
 process.  Although no information pertaining specifically to
 biodegradation of 1,2-trans-DCE  is available, results with
 similar compounds suggest that this process probably occurs
 but  at  a very slow rate.

   •* Photooxidation in the troposphere appears to be the dominant
 environmental fate of 1, 2-trans-DCS.  Once in the troposphere,
 the  compound is attacked at  the  double bond by hydroxyl  radicals,
 resulting in the formation of formic acid, hydrochloric  acid,
 carbon  monoxide, and formaldehyde.  The half-life of 1,2-trans-
 DCZ  in  the troposphere is estimated to be less than one  day.
 Given the properties of similar  compounds, photolysis of 1,2- trans
 DCS  in  aquatic systems and photodissociation in the terrestrial
 environment are probably insignificant.


 Health  Effects

     Very little information concerning exposure only to 1,2-
 trans-DCE is available.  There are no reports of carcinogenic
 or teratogenic activity by 1,2-trans-DCE in animals or humans.
 It is reportedly nonmutagenic in a variety of test systems.
Like other members of toe chlorinated ethylene series, 1,2-
 trans-DCE has anesthetic properties.  Exposure to high vapor
 concentrations has been found to cause nausea, vomiting, weak-
 ness, tremor, and cramps in humans.  Repeated exposure via
 inhalation of 800 mg/m  (8 hours/day, S days/week, for 16 weeks)
 was  reported to produce fatty degeneration of the liver in
 rats.   The intraperitoneal injection LD.n value for the rat
 is 1»S3i mg/kg.                        *°

     Although nephrotoxic and cardiac sensitising effects are
 associated with exposure to 1,1-dichloroethylene, the 1,2-DCE
 isomers have not been investigated with respect to this type
of effects.  1,2-trans-Oichloroethylene can inhibit aminopyrine
demethylatlon in rat liver microsomea in vitro, and it may
 thus interact with the hepatic drug-metabolising monooxygenase
system.


Toxicitv to Wildlife and Comes tic Animals

     Practically no information concerning the toxlcity of
1,2-trans-DCE to wildlife and domestic animals exists.  The
reported 06-hour LC.n value under static conditions is 135/000
ug/liter for the bllegill.  Under the same test conditions,
the LC.0 value for 1,1-dichloroethylene is 73,900 yg/liter.
Recommended criteria for protection of aquatic life are based
primarily on data concerning 1,1-dichloroethyltne.

 1, 2-trans-Dichloroethylene
Page 2
October 1S8S
                                                                  :/

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Regulations ano &cano*tc>i»

Aabient Water Quality Criteria  {USEPA}s

     The available data ar* not adequate for establishing criteria.

OSHA Standard!  790 mg/»3 TWA

ACGIH Threshold Liait Values!  750 rng/m3 TWA
                               1,000 «g/mj S.TBL


REFERENCES

AMERICAN COUNCIL Of GOVERNMENTAL INDUSTRIAL HVGISNISTS (ACGIH).
     1980.  Documentation of Threshold Liait Values.  4th ed.
     Cincinnati, Ohio.  488 pages

NATIONAL INSTITUTE FOR OCCUPATIONAL SAFETY AND HEALTH (NIOSH).
     1983.  Registry of Toxic Effects of Chemical Substances.
     Data Base.  Washington, D.C.  October 1983

SAX, N.I.  1975.  Dangerous Properties of Industrial Materials.
     4th ed.  van Hostrand Reinhold Co., New York.  1,258 pages

U.S. ENVIRONMENTAL PROTECTION AGENCY  (USEPA).  1979.  Water-
     Related Environmental Fate of 129 Priority Pollutants.
     Washington, D.C.  December 1979.  EPA 440/4-79-029

U.S. ENVIRONMENTAL PROTECTION AGENCY  (USEPA).  1980.  Ambient
     Water Quality Criteria for Dichloroethylenes.  Office
     of Water Regulations and Standards, Criteria and Standards
     Division, Washington, D.C.  October 1980.  EPA 440/5-80-041

U.S. ENVIRONMENTAL PROTECTION AGENCY  (USEPA).  1984.  Health
     Effects Assessment for 1,2-trans-Dichloroethylene.  Environments.
     Criteria and Assessment Office, Cincinnati, Ohio.   September
     1984.  BCAO-CIN-H041  (Final Draft)

WEAST, R.2., ed.  1981.  Handbook of Chemistry and Physics.
     62nd ed.  CRC Press, Cleveland, Ohio.  2,332 pages
1,2-trans-Dichloroethylene
Page 3
October 1985
                          2.0*}

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                        2,4-DICHLOROPHEKOL
 Summary
      2,4-Dichlorophenol (2,4-DCP)  la not very persistent in the
 envtronnent.  There la equivocal evidence suggesting that it may
 act as a tumor promoter*  Subcutaneous administration of 2,4-di-
 cftlorophenol to pregnant alee induced minor teratogenic effects.
 Chronic exposure caused nonspecific liver changes in alee.
 CAS Numbers   120-83-2
 Chemical Formulas   C.R.C
 IUPAC Name:   2,4-Dichlorophenol
 Important Synonyms and Trade Naaeii  2,4-DCP
 Chemical and Physical Properties
 Molecular Weight:   163.0
 Boiling.Points   210*C
 Melting point;   45»C
 Specific Gravitys   1.383 at 25*C
 Solubility in Waters  4,500 ng/liter
 Solubility in Organicsj  Soluble in benzene/ alcohol, ether,
                          and chloroform
 Log Octanol/Water  Partition Coefficient!  2.75
 Vapor Pressure:   0.12 ma eg at 20*C (calculated)
 Vapor Densityi   5.62
 pKai  7.4S
                          \
 Flash Pointi  114*C
 2,4-Dichlorophenol
 Page 1
 October 1985
Preceding page blank

-------
 Transport and Pate

      2,4-Diehlorophenol  (2,4-DCP)  is not very persistent in  the
 environment,  with  a half-life  of  about  1 week.   Degradation  by
 soil and water microorganisms  occurs readily  and appears to  be
 the  primary fats of 2,4-DCP.   However,  blodegradation  rates  are
 dependent'on a number  of  environmental  factors.   For example,
 degradation will proceed  much  more quickly  in systems  contain-
 in?  pollutant-adapted  microflora.   Volatilization and  adsorp-
 tion do not appear to  be  significant transport processes for
 2,4-*dicnlorophenol. Oxidation and hydrolysis are probably not
 important environmental fates.  Photodegradation of aqueous
 2,4-DCP is reported to occur under aerobic  conditions,  but it
 is unlikely that this  process  contributes significantly to its
 environmental fate. The  limited  data available  suggest that
 2,4-DCP does  not readily  bioaccumulate.


 Health  Effects

      No studies evaluating  the  carcinogenic potential  of 2,4-DCP
 are  available.  However,  one study provides evidence that this
 compound may  have  promoting activity*  Mice were initiated
 with skin applications of dimethyl-benzanthracene in benzene,
 and  then received  skin applications of  40.S ag/kg of 2,4-DCP
 two  times per week, for IS  or  24 weeks.   The  results indicated
 that 2,4-DCP  can act as a promoter in the production of papil-
 loraas.   However, the results must  be regarded as equivocal
 because of  limitations imposed  by  the experimental methods
 used in the study.

      2,4-DCP  is reported  to have some effects on mitosis and
 meiosis in  flower  buds and  root cells of Vicia faba.  No studies
 evaluating  the  mutagenic  activity  of DCP in other  eukayotic
 organisms or  bacteria  are available.  In alee, subcutaneous
 administration  of  74 mg/kg  2,4-DCP on days  6-14  of gestation
 resulted in a significant increase in abnormal fetuses,  with
 half of the anomalies  consisting of extended  legs.  Fetal mor-
 tality  was  unchanged,  but weights  were significantly lower
 than control!.  No other  report* of significant  teratogenic
 or reproductive effects are available.

     Very little information concerning  the acute  or chronic
 toxicity of 2,4-DCP is available.   Acute toxicity  following
 injection is  characterized  by  initial polypnea followed  by
 slowed  respiration  and dyspnea, hypotonia,  coma,  and death.
A maximum no-effect level of 100 rag/kg/day  was determined in
 a 6-month  feeding  study in  mice.   Only non-specific microscopic
 liver changes were  observed in  mice receiving 230  mg/kg/day.
 Intraperitoneal and oral  LDSO values of  430 mg/kg  and 580 mg/kg,
 respectively, are  reported  for  the rat.
2,4-Dichlorophenol
Page 2
October 1985
                                                                   - J

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Toxicity toWildlife and Domestic Animals

     Species nean acute values reported for the freshwater
species Oaphnia magna, fathead minnow, and bluegill are 2,605,
8,230, and 2,020 ug/liter» respectively.  \ chronic value of
36S ug/liter and an acute-chronic ratio of 23 are reported
for the fathead minnow.  The only information available con-
cerning saltwater species indicates that the mountain bass
Kuhlla sandvieensis exhibits a moderate reaction in response
to 20 rag/liter 2,4-DCP.  Complete destruction of chlorophyll
and 56.4% reduction of photosynthetic oxygen production are
observed after exposure of the freshwater alga Chlorella py-
renoidosa to 100 and 50 mg/liter, respectively.  The weighted
average bioconcentration factor for 2,4-DCP and the edible
portion of all freshwater and estuarine organisms consumed
by Americans is calculated to be 40.7.

     2,4-DO? residues have been detected in the liver and kidneys
oC cattle and chickens, and in chicken eggs.  Concentrations
of 2,4-DCP in animal tissues are reported to diminish rapidly
after withdrawal of the 2,4-DCP precursor, 2,4-diehlorophenoxy-
acetic acid  (2,4-D).  Mo information concerning toxicity of
2,4-DCP to domestic animals is available.


Regulations and Standards

Ambient Water Quality Criteria (USEPA):

     Aquatic Life

     The available data are not adequate for establishing criteria

     Human Health

     Health criterion:  3.09 mg/liter
     Organoleptic criterion:  0.3 ug/liter


REFERENCES

NATIONAL INSTITUTE FOR OCCUPATIONAL SAFETY AND HEALTH (NIOSH).
     1984.  Registry of Toxic Effects of Chemical Substances.
     Data Base.  Washington, D.C.  January 1984

SAX, N.I.  1975.  Dangerous Properties of Industrial Materials.
     4th ed.  Van Hoatrand Reinhold Co., New York.  1,258 pages

U.S. BNVIRONHENTAL PROTECTION AGENCY (BSEPA).  1979.  Mater-
     Related Environmental Fate of 129 Priority Pollutants,
     Washington, D.C.  December 1979.  EPA 440/4-79-029
2,4-Dichlorophenol
Page 3
October 1985
                               3J3

-------
U.S. ENVIRONMENTAL PROTECTION AGENCY  (USEPA) .  1980.  Ambient
     Hater Quality Criteria for 2,4-Dichlorophenol.  Office
     of Water Regulation* and Standards, Criteria and standards
     Division, Washington, D.C.'  October 1910.  EPA 440/5-80-042

WEAST, R.E., ed.  1981.  Handbook of Chemistry and Physics.
     62nd ed.  e*C Press, Cleveland, Ohio.  2,332 pages
2 f 4-Dichlorophenol
Page 4
October 1985

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                  2,4-DICHLOROPHENOXYACETlC  AGIO
Summary
     2,4-Dichlorophenoxyacetic acid (2,4-0) is a commonly used
broad spectrum herbicide,  it is a component of Agent Orange,
the defoliant most widely used in Vietnam,  it promoted tumors
after being painted on the skin of mice, and it probably is
a weak mutagen.  2,4-D caused developmental abnormalities and
was fetotoxic when administered to pregnant rats, mice, and
hamsters.  Dermal exposure to 2,4-D causes severe peripheral
neuropathy.


CAS Numbers  94-75-7

Chemical Formula:  Cl-C-H^OCHjCOOH

IUPAC Name:  2,4-Dichlorophenoxyacetic acid

Important Synonyms and Trade Names:  Agrotect, Dicotox, Phenox,
                                     2,4-D


Chemical and Physical Properties

Molecular Weight:  221.04

Boiling Point:  160'C at 0.4 ma 19

Melting Point:  138*C

Solubility in Water:  620 mg/liter

Solubility in Organics:  Soluble in organic solvents

Log- Octanol/Water Partition Coefficient!  2.5  (calculated)

Vapor Pressure:  <10   am Ig at 2S*C

Vapor Densityi  7.€3

pKa:  2.S


Transport and Pate

     Because of Its low vapor pressure and relatively high
solubility in water, 2,4-dichlorophenoxyacttic acid  (2,4-D) is
probably not very volatile.  In surface water, 2,4-D undergoes
either photolysis with oxidation to chlorophenols or photore-


2,4,-Dichlorophenoxyacetic acid
Page 1
October 1985                        '               Clamant

-------
                        - -_.-, *u*eri process occurs depends on
    pnysical properties of the media.  2,4-D is only weakly
adsorbed to soil and may leach Into groundwater, although studies
indicate that this is not an  important transport process.  Bio-
degradation by soil bacteria  may be an important fate process
for 2,4-D.


Health Effects

     2,4-Dichlorophenoxyaeetic acid has been assayed for car*
cinogenicity in rats, mice, and dogs.  Statistically significant
increases in tumor initiation have not been observed in any study.
Increases in the number of lymphosarcomas, total sarcomas,
and carcinomas in rats, however, suggest that it aay be carci-
nogenic.  A tumor-promoting effect was observed in a skin-paint-
ing study in mice.

     2,4-D has damaged DHA and inhibited DNA repair in several
strains of bacteria and yeast.  It caused chromosomal damage
and induced increased rates of sister chromatid exchange (SCE)
in cultured human lymphocytes.  2,4-D also induced SCE in Chinese
hamster ovary cells.  The results of the Drosophila sex-linked
recessive lethal assay were weakly positive.  2,4-D failed to
induce nutation in the Ames assay.  Considering all available
test data, 2,4-0 is a weak autagen.

     When administered to pregnant rats, nice, and hamsters,
2,4-D produces a pattern of developmental abnormalities, includ-
ing skeletal anomalies and cleft palate.  Fetotoxicity and
fetal death have also been reported.  The minimum level causing
major developmental abnormalities in rats is approximately
100 mg/kg.  No effect on reproduction wa* observed in a 3-gene-
ration rat study.

     2,4-D apparently is not very acutely toxic to humans,
with the average oral dose likely to be fatal estimated to
be 400 mg/Jcg.  However, considerable uncertainty exists regarding
what is a minimal toxic dose; it aay be as low as 80 ag/kg.
Symptoms of vomiting, fever, and profound muscle weakness are
usually reported after ingestion of 2,4-D.  2,4-D is irritating
to the eyes.  Absorption through the skin reportedly produces
severe peripheral neuropathy, with stiffness of extremities,
possible motor paralysis, and parathesia.

     The oral U>-5 for 2,4-0  in mice and rats is 375 mg/kg,
but the oral tD.J for dogs is 100 ag/kg.  Isters of 2,4-D have
comparable toxiclty.  Cardiac arrhythmia has been cited as a
cause of death in several acute studies.  Pathological changes
have also occurred in the gastrointestinal tract/ liver, lungs,
and kidneys.  The rabbit deraal LD5Q ii 1,400 ag/kg.
2,4,-Dichlorophenoxyacetic acid
Page 2
October 1985

-------
     Contrary to suggestions that 2,3,7fB-tetrachlorodibenzo-p-
dioxin contamination has contributed to th* toticity of 2,4-D,
no actual TCDD contamination of 2,4-D has b«tn reported, although
hexachlorodibenzo-p-dioxin and 2»7-dichlorodibenio-p-dioxin
have been found.  There is no experimental evidence that dioxins
are Corned by photolysis of 2,4-D.


Toxicitv to Wildlife and Domestic Animals

     Studies on the effects of exposure to 2f4-D and other
phenoxy herbicides on algae indicate that many single-celled
plants are not very sensitive to these compounds.  Concentra-
tions of 25 mg/liter 2,4-D administered for 10-12 days reduced
the growth rate of Scenedesmua, one of the more sensitive species,
by 421.  The growth of Hostol muscorun, a blue-green algae,
is inhibited at concentrations of 0.1 ag/liter.  Various forms
of filamentous algae, i.e., Chara, Hydrodictyon, and Pitophora,
are controlled at concentrations above 10 ag/liter.

     The 96-hour LD__ for Daphnia maqna is 2 mg/liter.  Concen-
trations of 2 mg/liter had ho detectable effect on shell growth
in oysters.

     2,4-D's toxicity to fish has been thoroughly studied.
The 24- and 48-hour LC.Q values for the bluegill were reported
to be S ag/liter foe 274-D.  Esters of 2,4-D are slightly more
toxic.  Concentrations of SO mg/liter had no observable effect
on tadpoles of the frog, Rana tenporaria.

     Animal poisonings have been reported and attributed to
herbicide formulations containing 2,4-D, but in most instances
a definite causal relationship has not been established.  2,4-D
does not bioaccumulate in the adipose tissue.


Regulations and Standards

OSHA Standards  10 mg/m3 TWA

ACGII Threshold Limit Value:  10 mg/m3 TWA


REFERENCES

AMERICAN CONFERENCE OF GOVERNMENTAL INDUSTRIAL HYGIENISTS (ACGIH}.
     1980.  Documentation of the Threshold Limit Values.  4th
     ed.  Cincinnatir Ohio.  488 pages

INTERNATIONAL AGENCY FOR RESEARCH ON CANCER (IARC),  1977.
     IARC Monographs on the Evaluation of the Carcinogenic
     Risk of Chemicals to Man.  Vol. 15:  Some Fumigants, the
2,4,-Dichlorophenoxyacetic acid
Page 3
October 1985
                                                  Cl*rn«nt AMOCUKM

-------
     Herbicides, 2,4-0 and 2,4,5-T, Chlorinated Dibenzodioxins
     and Miscellaneous Industrial Chemicals.  World Health
     Organization, Lyon, France

LYMAN, W.J., REEHL, W.F., and ROSENBLATT, D.H.  1982.  Handbook
     of Chemical Property Estimation Methods;  Environmental
     Behavior of Organic Compounds.  McGraw-Hill Book Co.,
     Hew York

THE M£RCK INDEX.  1976.  9th ed.  Windholz, M., ed.  Merck
     and Co., Rahwsy, New Jersey

SAX, N.I.  1975.  Dangerous Properties of Industrial Materials.
     4th ed.  Van Nostrand Reinhold Co., New York.  1,258 pages

U.S. ENVIRONMENTAL PROTECTION AGENCY (DSEPA).  1979.  Water-
     Related Environmental Fate of 129 Priority Pollutants.
     Washington, D.C.  December 1979.  EPA 440/4-79-029

VERSCHUEREN, I.  1977.  Handbook of Environmental Data on Organic
     Chemicals,  van Nostrand Reinhold Co., New York.  659 pages

VETERANS ADMINISTRATION.  1984.  Review of Literature on Herbi-
     cides, Including phenoxy Herbicides and Associated Diaxins.
     Vols. 1-IV.  Department of Medicine and Surgery, Washington,
     D.C.
2,4,-Dichlorophenoxyacetlc acid
Page 4
October 1985

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                       1,2-DICHLOROPROPANE
Sum-nary
     1,2-Dichloropropane  Increased  the Incidence of combined
adenomas and carcinomas of the liver when administered to rats
and mice, and it was found to be nrutagenic using the Ames assay,
High concentrations can depress the central nervous system
and adversely affect the  liver, kidneys, adrenals, and heart.
CAS Number:  78-87-5
Chemical Formula:  CHjClCHClCH-j
IUPAC Name:  1,2-Dichloropropane
Important Synonyms and Trade Names:  Propylenecbloride, propylene
                                     dichloride
Chemical andPhysicalProperties
Molecular Weight:  112.99
Boiling pointi  §f.S*C
Melting Pointi  -100*C
Specific Gravityt  1.16 at 20*C
Solubility in Watert  2,700 mg/liter at 20«C
Solubility in Organic**  Miscible with organic solvents
Log Octanol/Water Partition Coefficientt  2.28
vapor Pressures  42 ma Hg at 20*C
Vapor Density:  3.9
Flash Pointt  21*C (open cup)

Transport and Pate       v
     Volatilization and subsequent photooxidation are probably
important environmental fate processes for 1,2-diehloropropane.
In surface water and soil, hydrolysis may also be a significant

1,2-Dichloropropane
Page 1
October 1985

-------
 fate process, especially if  the compound is adsorbed onto clay
 particles.  Soil microbes can biodegrade 1,2-dichloropropane,
 but this  is likely to occur  more slowly titan volatilization.
 1,2-Dichloropropane is probably only moderately persistent
 in the environment.


 Health Effects

     1,2-Dichloropropane caused an  increased incidence of com-
 bined-adenomas and carcinomas of the liver in male and female
 nice and  caused a slight increase in mammary adenocarcino>nas
 in female rats (NT? 1984).,  In an earlier study, 80 C3H mice
 were exposed to 1,850 mg/m   of 1,2-dichloropropane for 4 to
 7 hours per day 37 tines and were then observed for the next
 7 months; only 3 nice survived, but all of these developed
 multiple  hepatomas (Heppel et al. 1948).  1,2-Dichloropropane
 was found to be mutagenic using the Ames assay both with and
 without metabolic activation.  It also increased the frequency
 of 8 araguanine-resistant mutants in the Aapergillus nidulans
 spot test.  Ho information was available on the reproductive
 or teratogenic effects of this compound.

     High concentrations of  1,2-dichlocopropane cause central
 nervous system depression and narcosis in humans.  Other human
 symptoms  include headache, vertigo, lacrimation, and irritation
 of the aucous membranes.  Studies indicate that exposure to
 high concentrations may affect the  rate of growth in rats and
 guinea ;igsf and cause fatty degeneration and multilobular
 or centrilobular necrosis of the liver.  Hlstopathological
 changes were also observed in the kidneys, adrenals, and heart.
 1,2-Dichloropropane is a mild skin  Irritant.  It is moderately
 irritating to the eye but does not cause permanent injury.

     The oral t»D.n for rats  is 1,900 mg/kgi the oral LD-~ for
 mice is 360 mg/kf.  The dermal L05Q foe rabbits is 8,750umg/kg.


 Toxicity to Wildlife and Domestic Animals

     Only limited data are available on the effects of 1,2-
 dichloropropane on wildlife  and domestic animals.  The 48-hour
EC.rt is 52 eg/liter in Daphnia magna.  The 96-hour lC-a for
 thiubluegill is 300 og/litar; for the fathead minnow,3It is
 139.3 mg/liter; and for the  tidewater sliverside it is 240 mg/liter
 In an embryo-larval test using the  fathead minnow, chronic
 effects developed at 8,100 tig/liter.
1,2-Dichloropropane
Page 2
October 1985

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Regulations ana stanoacas

Ambient Water Quality Criteria  (USEPA):

     The available data act not adequate foe establishing cri-
     teria.

OSHA Standard  (air):  350 mg/ra3 TWA

AC3IH Threshold Limit Values:  350 mg/m^ TWA
                               510 mg/m-1 STEL


REFERENCES

AMERICAN CONFERENCE OP GOVERNMENTAL INDUSTRIAL HYGIENISTS (ACGIH).
     1980*  Documentation of the Threshold Limit Values.  4th
     ed.  Cincinnati, Ohio,  488 pages

HEPPEL, L.A., HIGHMAN, B., and PEAKS, E.G.  1948.  Toxicology
     of 1,2-dichloropropane (propylene dichloride):  rv. Effects
     of repeated exposures to a low concentration of vapor.
     J. Ind. Hyg. Toxicol. 30:189-191

THE MERCK INDEX.  1976.  9th ed.  Windholz, M., ed.  Merck
     and Co., Rahway, New Jersey

NATIONAL INSTITUTE FOR OCCUPATIONAL SAFETY AND HEALTH (NICSH).
     1984.  Registry of Toxic Effects of Chemical Substances.
     Data Base.  Washington, D.C.  October 1984

NATIONAL TOXICOLOGY PROGRAM (HtP).  1984.  Annual Plan for
   •  Fiscal Year 1984.  National Toxicology Program, Public
     Health Service, Department of Health and Human Services,
     Department of Health and Human Services.  February 1984
     NTP-84-023

SAX, N.I.  1975.  Dangerous Properties of Industrial Materials.
     4th ed.  Van Hostrand Reinhold Co., New York.  1,258 pages

O.S. ENVIRONMENTAL PROTECTION AGENCY (USEPA).  1979.  Water-
     Related Environmental Fate of 129 Priority pollutants.
     Washington, D.C.  December 1979.  EPA 440/4-79-029

U.S. ENVIRONMENTAL PROTECTION AGENCY (USEPA).  1980.  Ambient
     Water Quality Criteria for Dichloropropanes/propenes.
     Office of Water Regulations and Standards, Criteria and
     Standards Division* Washington, D**C.  October 1980.  EPA
     440/5-80-043

VEASCHUEREN, K.  1977.  Handbook of Environmental Data on Organic
    ' Chemicals.  Van Nostrand Reinhold Co., New York.  659 pages


1,2-Dichloropr opane
Page 3
October 1985

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 WEAST,  R.E.,  td.   1981.  Handbook of Ch«»istry and Physics.
      62nd ad.   CRC Press, Cleveland, Ohio.  2,332 pages
1,2-Dichloropropane
Page 4
October 1985

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                        1,3-DICHLOROPROPENE
Summary
     1,3-Dichloropropene  is moderately persistent  in soils
but less persistent in water,.  No complete carcinogenicity
studies are currently available/ but cis-l,3-dichloropropene
caused injection-site sarcomas in mice and was found to be
mutagenic using the Ames  assay.  Chronic exposure  caused liver
and kidney damage.
CAS Number:  542-75-6

Chemical Formulas  CBC1CBCH2C1

IUPAC Namei  1,3-Dichloro-l-propene

Important Synonyms and Trade Names:  1,3-Dichloropropylene,
                                     Telone, DCP


Chemical and Physical Properties

Molecular Weight:  110.97

foiling points  1Q4«C (cis)
                112«C (trans)

Melting Points  No available data

Specific Gravity:  1.217 at 2Q*C  (cia)
                   1.224 at 20*C  (trans)

Solubility in Waters  2,700 tag/liter at 25*C

Solubility in Organicsi  Soluble  in ether, benzene, and chloroform

Log Octanol/Water Partition Coefficient:  1.98

Vapor Pressures  28 ma Hg at 25"C

Vapor Density*  3.83


Transport and Fate

     1,3-Dichloropropene (DC?) is moderately persistent in
soils but less persistent in water.  Volatilization from soil
and water into the atmosphere, where it is subsequently degraded


1,3-Dichloropropene
Page 1
October 1985
                                                           •ooatao

-------
 by  photooxidation,  is probably  the predominant  transport  and
 fata mechanism  for  DCP.  Although no  information was  found
 on  the  adsorption of 1,3-dichloropropen*  in  aquatic systems,
 sorption  to  soil organic* is an important  terrestrial process
 and accounts for the persistence of DCP in soils.  Hydrolysis
 of  adsorb**  material in soil and water to  product  3-chloroallyl
 alcohol occurs  rather slowly but may  be an important  fat* pro-
 cess.   Biodegradation of DCP also occur* slowly* but  soil bac-
 teria ar* probably  responsible  for the degradation of the
 3-chloroallyl alcohol to carbon dioxide and  water.
     * *
    *
 Health  Effects

     A  carcinogenicity bioassay of 1,3-dichloropropen*  is being
 conducted by the National Toxicology  Prograa.   No  carcinogenicity
 studies are  currently available, but  cis-l,3-dichloropropene
 caused  application-site sarcomas in aic* following subcutaneous
 injection, and  the  chemical was mutagenic  in the Ames assay.
 No  information  on the teratogenicity  or reproductive  toxicity
 of  1,3-dichloropropene was found in the literature reviewed.
 Chronic exposure caused liver and kidney toxicity  at doses
 as  low  as 13.6  mg/m .  However,  after a 3-month recovery period,
 exposed animals showed no ill effects.  The  oral LD-. value
 in  the  rat is 250 mg/kg.                           *°


 Toxicity  to  Wildlife and Domestic Animals

     Acute Z>C.Q values for aquatic organisms exposed  to 1,3-di-
 chloropropen*9wer*  about 6,000  yg/lit«r in two  freshwater spe-
 cies, 1,770  ng/liter in a saltwater fish,  and 790  ug/lit«r
 in  a saltwater  invertebrate.  Only on* chronic  toxicity tert
 on  1,3-dichloropropen* was reported.  This indicated  that di-
 chloropropen* was toxic at levels of  244 ug/liter  to a freshwater
 fish species.

     Ho information on the toxicity of 1,3-dicbloropropene
 to  terrestrial  wildlif* or domestic animals  was found in the
 sources reviewed*


 Regulations  and Standards

Ambient Water Quality Criteria  (USEPA)i

     Aquatic Life

     The  available  data ar* not  adequate for establishing criteria,
     However, SPA did report th* lowest values  known to cause
     toxicity in aquatic organism*.
1,3-Dichloropropene
Pag* 2
October 1985
                                                                      J

-------
         Acute toxicityi  6,060
         Chronic toxicityi  244 ug/liter

     Saltwater

         Acute toxicity;  790
         Chronic toxicity:  No available data

     Human Health

     Criterion:  87 Mg/liter

ACGIH Threshold Limit Valuesj  5 mg/m3 TWA
                               50 ag/ar STEL


REFERENCES

AMERICAN CONFERENCE OF GOVERNMENTAL INDUSTRIAL EYGIENISTS  (ACGIH),
     1980.  Documentation of the Threshold Limit Values'. ' 4th ed.
     Cincinnati, Ohio.  488 pages

NATIONAL INSTITUTE FOR OCCUPATIONAL SAFETY AND HEALTH  (NIOSH).
     1984.  Registry of Toxic Effects of Chemical Substances.
     Data Sase.  Washington! D.C.  April 1984

U.S. ENVIRONMENTAL PROTECTION AGENCY (USEPA).  1979.  Hater-
     Related Environmental Fate of 129 Priority Pollutants.
     Washington, D.C.  December 1979.  SPA 440/4-79-029

0.5. ENVIRONMENTAL PROTECTION AGENCY (USEPA).  1980.  Ambient
     Water Quality Criteria for Dichloropropanes/propenes.
     Office of Water Regulations and Standards, Criteria and
     Standards Division, Washington, D.C.  October 1980.  EPA
     440/5-80-043

VAN DUUREN, B.L., GOLDSCHMIDT, B.M., LOEWENGART, G., SMITH,
     A.C., MELCH10NNE, S., SEIDMAN, X., and ROTH, D.  1979.
     Carcinogenicity of halogenated olefinic and aliphatic
     hydrocarbons in mice.  JNCI 63:1433

VERSCHUEREN, K.  1977.  Handbook of Environmental Data on Organic
     Chemicals.  Van Nostrand Reinhold Co., New York.  659 pages

WEAST, R.E., td.  1981.  Handbook of Chemistry and Physics.
     62nd ed.  CRC Press, Cleveland, Ohio.  2332 pages
1,3-Dichloropropene
Page 3
October 1985

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                              DICOFOL


 Summary

      Dicofol  (Kelthane) is in organochlor ine pesticide that  is
 moderately persistent In the environment.  In an NCI carcinogen*
 ieity bioassay, It produced hepatocellular carcinomas in male
 mice, but not in rats or female mice.  Dicofol caused anomalies
 in the third-generation offspring in one study on alee but not
 in another.  It also had reproductive effects in rats and mice.
 Chronic exposure produced liver lesions in rats.


 CAS Humbers  115-32-2

 Chemical Formulas  Cj,I»OCl-

 IUPAC Name:  2,2,2-Trichloro-l ,1-bis (4-chlorophenyl) ethanol

 Important Synonyms and Trade Hames:  Kelthane, Acarin, Hitigan


 Chemical and Physical properties

 Molecular Weight:  441.5

 Boiling Point:  Not available in literature reviewed

 Melting Point:  79*C

 Specific Gravity:  1.130 at 20°C

 Solubility in Water:  590 ng/ liter at 20*C
 Solubility in Organics:  Soluble in most aliphatic and aromatic
                          solvents

 Log Octanol/Water Partition Coefficient:  5.56

 Plash Point:  49»C (closed cup)


 Transport and Fate

      Little information was found on the transport and fate
 of dicoflol in the environment.  It in one of the less persistent
 organochlorine pesticides and disappears fairly readily from
 soil.  However, trace amounts will persist for up to 1 year.
 Volatilization Is probably the primary transport mechanism,
 as movement through soil is probably limited by low water solu-
 bility and binding to soil material.  Based on results for


 Dicofol
 Page 1
 October 1985

                                                 DCiemane Ammocmtmm


Preceding page blank

-------
DDT, dicofol  is probably biodegraded by soil bacteria,  and
this say be the most  important fate process in  foil.  In  aquatic
systems, sorption to  sediments is probably an iaportant fate,
and bioaccuaulation aay also be  important.


Health Effects

     Dicofol  caused hepatocellular carcinoaaa in male aice
but not in female aice nor in rats of either sex (NCI 1978}.
In a three-generation study, continuous feeding of 7 ppra  (approx-
imately 0.8 mg/kg) dicofol to aice resulted in  anomalies  in
offspring of  the third generation.  However, in a five-genera*
tion study, Brown (1971) noted no fetal anomalies in aice fed
up to 500 ppra (approximately €0  mg/kg) dicofol  in their diets.
Only litter size, weight, and viability decreased significantly
at this concentration.  Brown  (1971) also reported that rats
did not produce offspring if fed aore than 100  ppra  (approximately
5 mg/kg) in their diets.  Dicofol was not autagenic in  several
aicrobial test systems.

     In a 2-year study in rats,  faith et al.  (1959) noted that
liver lesions were seen in animals administered acre than 1,000 pp
(approximately 45 mg/kg) in their diets and that growth decreased
in animals fed diets containing  more than 500 ppa  (approximately
23 mg/kg) dicofol.  The acute oral LD.Q in rats was 800 rug/kg
for aales and $80 mg/kg for females.


Toxicity to Wildlife and Domestic Animals

     The LC.0 for rainbow trout  exposed to dicofol for  48 hours
was 100 mg/Ilter.  The 48-hour &C.. values for Daphnia  magna
and stone flies were 390 and 3,000 af/liter, respectively.
Fathead ainnows bioconcentrate dicofol to a level 10,000  tiaes
that found in water, with a steady-state concentration  occurring
in 40 to 60 days (Eaton et al. 1983).

     The toxieity of dicofol has been studied in several  wild
bird species.  The LC.Q values for 2-week-old birds fed contami-
nated feed for 5 days were 1,500 ppa for coturnix, 3,000  ppa
for bobwhites, 2,300 for pheasants, and 1,900 for mallard ducks.
No inforaation was found on the  toxieity of dicofol to  other
terrestrial wildlife or to doaestie aniaals.
REFERENCES

BROWN, J.R.  1971.  The effect of dietary lelthane on mouse
     and rat reproduction.  In Tahori, A.S., ed.  Proceedings
     of the 2nd International Congress on Pesticide Chemicals,
     Gordon and Breach, New York.  Vol.  6,  pp. 531-548
Dieofol
Page 2
October 1985

-------
                               _ w*aj on LIioconcentr&ti.on oc
     Kelthane In fathead minnows.  Arch. Environ. Contain. Toxicol,
     12:439-445

EXECUTIVE OFFICE OF THE PRESIDENT.  1971.  Ecological Effects
     of Pesticides on Non-Target Species.  Office of Science
     and Technology, Washington, D.C.  June 1971.  EOP/OST-71

FARM CHEMICALS HANDBOOK.  1984.  70th ed.  Meister, R.T., ed.
     Meister Publishing Co., Willoughby, Ohio

INTERNATIONAL AGENCY FOR RESEARCH ON CANCER (IARC).  1983.
     IARC Monographs on the Evaluation of Carcinogenic Risk
     of Chemicals to Humana.  Vol. 30:  Miscellaneous Pesticides.
     World Health Organization, Lyon, France.  Pp. 87-101

NATIONAL CANCER INSTITUTE (NCI).  1978.  Bioassay of Dicofol
     for possible Carcinogenicity.  (CAS No. 115-32-2)  NCI
     Carcinogenesis Technical Report Series No. 90.  Washington,
     D.C.  DHEW Publication No.  (NIH) 78-1340

NATIONAL INSTITUTE FOR OCCUPATIONAL SAFETY AND HEALTH (NIOSH).
     1934.  Registry of Toxic Effects of Chemical Substances.
     Data Base.  Washington, D.C.  July 1984

SMITH, R.B., Jr., LARSON, P.S., FINNEGAN, J.E., BAAG, H.R.,
     HENNIGAR, G.R., and COBEY, F.  1959.  Toxicologic studies
     on 2,2-bis-(chlorophenyl)-2,2,2-trichloroethanol (Kelthane}.
     Toxicol. Appl. Pharmacol. Is 119-134

U.S. ENVIRONMENTAL PROTECTION AGENCY (USEPA).  1979.  Water-
     Related Environmental Fate of 129 Priority Pollutants.
     Washington, D.C.  December 1979.  EPA 440/4-79-029

VERSCHUEREN, K.  1977.  Handbook of Environmental Data on Organic
    'Chemicals.  Van Nostrand Reinhold Co., New York.  659 pages

WEAST, R.E., ed.  1981.  Handbook of Chemistry and Physics.
     62nd ed.  CHC Press, Cleveland, Ohio.  2,332 pages

WORTHING, C.R., ed.  1979.  The Pesticide Manual:  A World
     Compendium.  British Crop Protection Council, Croydon,
     England.  655 pages
Dicofol
Page 3
October 1985

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                        DIETHYL PHTHALATE
            iT1
Su nonary
     Oiethyl phthalate  (DBF) has not been  shown  to be  carcino-
genic, but  it was  found to be mutagentc  using bacterial  test
systems.  Intraperitoneal administration to pregnant rats  induces
adverse reproductive effects.  The chronic toxicity of diethyl
phthalate is low.
CAS Number:  34-66-2
Chemical Formulas  ci2H14°4* CfiH4
IUPAC ^ame:  Diethyl ester phthalic acid

Ch€nica'lv, and Phys teal ?roper ties
Molecular Weight}  222.24
Boiling Point}  298*C
Melting Points  -40.5*C
Specific Gravityt  1.1175 at 20*C
Solubility in Waters  896 mg/liter at 25°C
Solubility in Organicss  Soluble in acetone and benzene; raiseible
                         with alcohol, ether, ketones, and esters
Log Qctanol/Water Partition Coefficient:  3.22 (calculated)
Vapor Pressures  0.05 mm Hg at 70*C
Flash points  162.7i*C

Transport and Fate
     Much of the information concerning the environmental move-
ment and fate of diethyl phthalate (DS?) is derived from data
for phthalate esters in general.  DEP probably hydrolyzes in
surface waters, but at such a flow rate that this process is not
environmentally significant under most conditions.  Photolysis
and oxidation do not appear to be important environmental fate
processes.  Volatilization is not an important environmental
transport process for DEP in natural waters.  However, there

Diethyl phthalate
Page 1
October 1915
                                                   Ctemyie A»«ociaE«e
 Preceding page blank

-------
 is evidence that It can be  slowly volatilized (torn DSP-containing
 materials at relatively high temperatures.   Consequently,  some
 atmospheric dispersion of DEP due to vaporization during manu-
 facture,  use,  or waste disposal  probably occurs.

      Adsorption onto suspended solids and partieulate  matter,
 and complex* tion with natural organic substances  are probably
 the moat  important environmental transport  processes for DEP.
 The octanol/water partition coefficient  for 06? suggests that
 this compound  would be adsorbed  onto particulates high in  organic
 matter.   This  contention is supported by the fact that phthalate
 es tar's  are commonly found in freshwater  and saltwater  sediment
 samples.   DEP  can be dispersed to aquatic and terrestrial  systems
 by coraplexation with natural organic substances.   It readily
 interacts with the fulvic acid present in humic substances
 in water  and soil, forming  a complex which  is very soluble
 in water.

      A  variety of unicellular and multicellular organisms  take
 up and  accumulate phthalate esters,  and  bioaccumulatlon of
 OS? is  considered an important fate  process,  Biodegradation
 is also considered an Important  fate process for  DBF in aquatic
 systems and soil.  Because  phthalate esters, and  presumably
 DIP,  are  degraded under most conditions  and can be metabolized
 by multicellular organisms, it is unlikely  that long-term  bio-
 accumulation or bioaagnif ieation occurs.

      Analysis  using BFA*s Exposure Analysis Modeling system
 suggests  that  for DBF, chemical  and  biochemical transformations
 will  compete favorably in ecosystems with long retention times,
 such  as ponds  and lakes.  If input of DEP remains constant,
 its concentration is expected to approach a steady state,   if
 input stops, Its concentration is expected  to decrease relatively
 quickly.   Transport is the  dominant  process for DBF la rivers,
 and the oceans are the ultimate  sink in  these ecosystems.


 Health  affects

      There are no reports that DEP is carcinogenic in  animals
 or humans.   However, DBF is reported to  be  mutagenic in bacterial
 test  systems (Seed 1912).   Reduced fetal weight,  resorptiona
 and dose-related ausculoskeletal abnormalities were observed
 among fetuses  front rats exposed  intraperitoneally to DBF during
 gestation.
                         %
      The  acute toxicity for laboratory animals by most routes
 of administration is very low.  Oral, inhalation, and  Intraperi-
-toneal LD,fl values of 9,000 mg/Xg, 7,510 ag/» , and 5,058  mg/kg
 respectively,  are reported  for the rat.   The no-effect levels
 determined from chronic feeding  studies  of  six or more weeks
 duration  are 2,300 ng/kg/day for the rat, and 1,250 mg/kg/day


 Diethyl phthalate
 Page  2
 October 19S5
,

-------
COC &ne auy i wiw.i uu »^itr ^ A L i. <_ 4«si
-------
3*EO» J.L.  1982.  Mutagenic activity of phthalate esters in
     bacterial liquid suspension assays.  Environ. Health Per-
     Spect,  45:111-114

U.S. ENVIRONMENTAL PROTECTION AGENCY (USEPA).   1979.  Water-
     Related Environmental Pate of 129 Priority Pollutants.
     Washington, D.C.  December 1979.  EPA 440/4-79-029

U.S. ENVIRONMENTAL PROTECTION AGENCY (USEPA) .   1980.  Alibi en t
     Water Quality Criteria for Phthalate Esters.  Office of
     Water Regulations and Standards, Criteria and Standards
     Division, Washington, D.C.  October 1980.  EPA "440/5-80-067

WEAST* R.E., ed.  1931.  Handbook of Chemistry and Physics.
     62nd ed.  C1C Press, Cleveland, Ohio.  2,332 pages
Diethyl phthalate
Page 4
October 1935

-------
 Summary
     Diisobutyl  ketone  i§ mildly  irritating to  the ayes, nose,
 throat,  and  akin in humans.  Inhalation exposure to high concen-
 trations increased liver and kidney weights in  rats and guinea
 pigs.
 CAS Number:  108-83-8
 Chemical Formula:   (CChj) jCHCHjJ jCO
 IUPAC Name:  2,5-Dimethyl-4-heptanone
 Important Synonyms and Trade Names:  Isobutyl ketone

 Chemical and Physical Properties
 Molecular Height:  142.2
 Boiling  Point:   1SS*C
 Melting  Point:   -41.5"C
 Specific Gravity:  0.81 at 20'C
 Solubility in Mater:  500 mg/liter
 Solubility in Organics:  Niscible with most organic liquids
 Log Octanol/Water Partition Coefficient;  2.8 (calculated)
 Vapor Pressure:   1,7 no Hg at 20*C
 Vapor Density:   4.9
 Flash Point:  60»C

 Transport and fate
     Ho  information on the transport and fate of diisobutyl
 ketone was found  in the literature reviewed.  Based on its
 chenical and physical properties, the compound probably is
 not very volatile.  It aay be adsorbed by soil organics and
 sediment to some  degree*  Xetones in general react in acidic
media to form secondary alcohols*  This reaction would probably
 occur in natural  waters with low pH.  Ketones are not likely
 to be very persistent in the environment.
Diisobutyl ketone
Page 1
October 1985
                                                         Ammocmtmm

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Health Effects

     Biisobutyl ketone is not very toxic to humans or laboratory
animals.  It does not appear to be carcinogenic, autagenic, or
teratogenic.  A 3-hour exposure by human volunteers to 290 and
580 mg/m  slightly irritated the eyes, nose, and throat.  In
another study of volunteers, some eye irritation and unpleasant
odor *43 reported at concentrations above 145 mg/m .  Diiso-
butyl ketone is also mildly irritating to the akin.

     Rats and guinea pigs were exposed by-inhalation for 7 hours
at varying concentrations.  At 1,450 mg/nr the liver and kidney
weights of female rats increased.  Concentrations above 2,030 mg/ra
caused an Increase in liver and kidney weights in both sexes,
with mortality occurring at the 9,583 ag/a3 level.  An 8-hour
inhalation exposure to 11,615 «g/aj killed S out of 6 rats.
The rat oral LD,n is 5,750 ag/kgi the rabbit dermal LD-n is
17 g/kg.       50                                     50


Toxicif/ to Wildlife and Domestic Animals

     No information on the toxicity of diisobutyl ketone to
wildlife and domestic animals was available in the sources
reviewed.


Regulations and Standards

NIOSH Recommended Standard (air)s  140 ag/a3 TWA

OSHA Standard (air);  309 mg/ra3 TWA

ACGIH Threshold Limit Value:   150 ag/a3 TWA


REFERENCES

AMERICAN CONFERENCE OF GOVERNMENTAL INDUSTRIAL HYGIENISTS (ACGIH).
     1980.  Documentation of the Threshold Liait Values.  4th
     ed.  Cincinnati, Ohio.  488 pages

DOOLL, 3.t XLAA33ZN, C.D., and AMDOR, M.O., eds.  1980.  Casarett
     and Doull's Toxicology!   The Basic Science off Poisons.
     2nd ed.  Macnillan ^Publishing Co., Netr York.  778 pages

LYMAN, W.J., REEHL, W,P., and ROSENBLATT, D.R.  1982.  Handbook
     of Cheaical Property Estimation Methods:  Environmental
     Behavior of Organic Compounds.  McGraw-Hill Book Co.,
     Sew York                                   .
Diisobutyl ketone
Page 2
October 1985

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THE MERCK INDEX.  1976.  9th td.  Windholz,  K.,  ed.   Merck
     and Co., Rahway, New Jersey

NATIONAL INSTITUTE FOR OCCUPATIONAL SAFETY AND HEALTH (NIOSH).
     1984.  Registry oC Toxic Effects of Chemical Substances.
     Data Base.  Washington, D.C.  October 1984

SAX, N.I.  1975.  Dangerous Properties of Industrial  Materials.
     4th ed.  van Nostrand Reinhold Co., New York*  1/258  pages

VERSCHUEREN, K.  1977.  Handbook of Environmental Data  on  Organic
     Chemicals.  Van Nostrand Reinhold Co./  New  York.   639 pages

WEAST, I.E., ed.  1981.  Handbook of Chemistry and Physics.
     62nd ed.  CRC Press, Cleveland, Ohio.  2,332 pages
Diisobutyl ketone
Page 3
October 1985

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                  DIMETHYLAMINOETHYL METHACRYLATE
 Summary
      Dinethylaminoethyl methacrylate is  irritating to  the skin,
 eyes, and mucous membranes and is a strong lachrymator.

 CAS Numbers  2867-47-2
 Chemical Formula:  CH2C {CH3>COOOi2CH2N (CH3> 2
 IUPAC Same:  2-9imethylaminoethyl-2-raethylpropenoate
 Important Synonyms and Trade Names:  2-Dimethylaninoethyl
                                      methacrylate

 Chemical and Physical Properties
 Molecular Weights  157
 Boiling Point:  187*C
 Specific Gravity*  0.933 at 25«C
 Solubility in Water:   Soluble in water
 Solubility in Organicss  Soluble in organic solvents
 Vapor Density:  5.4
 Flash Point:  74*C (open cup)

 Transport and Fate
      Ho information on the transport and fate of dimethylamino-
 ethyl raethacrylate was available in the sources reviewed.

 Health Effects
      Only Halted data on the toxicity of diaethylaminoethyl
 methacrylate were found in the literature searched.  The compound
 is an irritant to the akin, eyes, and mucous membranes, and
 it is a strong lachrymator.  The oral and inhalation t»D-Q values
 for the rat are 1,750 mg/kg and 620 ng/m /4 hours, respectively.
 Dimethylaitinoethyl methacrylate
 Page 1
 October 1985
Preceding page blank

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Toxicity to Wildlife and Domestic Animals

     Mo information on the toxicity of dinethylarainoethyl metha-
ccylate to wildlife and domestic animals was found in the sources
reviewed.


Regulations and Standards

     Ho regulations or standards have been established foz
dimethylaminoethyl nethacrylate.


REFERENCES

HATIQSAL INSTITUTE FOR OCCUPATIONAL SAFETY AHO HEALTH (MIOSH).
     1984.  Registry of Toxic Effects of Chemical Substances.
     Data Base.  Washington, D.C.  October 1984

SAX, N.I.  1975.  Dangerous Properties of Industrial Materials.
     4th ed.  Van Nostrand Reinhold Co., Hew York.  1,258 sages

VERSCHUERSN, K.  1977.  Handbook of Environmental Data on Organic
    'Chemicals.  Van Mostrand Reinhold Co., Hew York.  659 pages

WEAST, I.E., ed.  1981.  Handbook of Chemistry and Physics.
     62nd ed.  CRC Press, Cleveland, Ohio.  2,332 pages
Dinethylaminoethyl aethacrylate
Page 2
October 198S
                                                                  j

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                         DIMETHYLAHII.I8E
Summary
     Dimethylaniline  la a central nervous ays ten depressant,
and  it can cause tremors, convulsions* slowed respiration,
and  death dye  to respiratory paralysis.  Acute occupational
exposure has caused intense abdominal pain, unconsciousness,
and  visual disturbances.  As little as 50 mg/fcg was shown to
be lethal in humans.
CAS  Numbers  121-69-7
Chemical Formula;  CgH.tHCBj).
IUPAC Name:  N,N-Oinethylaniline
Important Synonyms and Trade Names:  N,N-Dimethylbenzeneamine,
                                     dimethylphenylamine,
                                     a-phenyldimethylaraine
Chemical and fhysJLcal Properties
Molecular Weight:  121. IS
Boiling Points  193. 1*C
Melting Points  2.5»C
Specific Gravity:  0.9557 at 20*C
Solubility in Waters  Slightly soluble
Solubility in Organics:  Soluble in alcohol, chloroform, and ether
Log  Octano I/Water Partition Coefficients  2*62
Vapor Pressures  1 mm Hg at 29.5*C
Vapor Densitys  4.17
Flash Point;  €1*C

Transport and Fate
     Virtually no information on the environmental transport
and  fate of dimethylaniline is available.  Although some vola-
tilization of this compound can occur, it probably is not a

Dimethylaniline
Page 1
October 1985

-------
 sifnifleant  transport process.  Because  it  is  soluble  in organic
 compounds  and has a moderate log octanol/water partition coeffi-
 cient, adsorption to organic particulatea in coil or bed sediments
 •a/  affect dimethylaniline's transport in environmental media.
 Some bioaccuaulation of  this compound aay also occur.  The
 available  data are not adequate to characterize the importance
 of biodegradation or other fate processes.


 Health affects

     Relatively little information on the toxicity of dimethyl-
 aniline  is available.  There are no reports of carcinogenic,
 mutagenic, or teratogenie activity by this compound in hu-oans
 or animals.  The physiological effects of dimethylaniline have
 been compared to those of aniline, although the former is thought
 to be quantitatively less toxic.  Toxic  effects aay be produced
 as a result  of ingestion, inhalation, or absorption through
 the  skin*  Dimethylaniline is reported to induce aethemoglobin
 formation  in dogs after  single oral doses of 50 ag/kg.  This
 compound is  a central nervous systea depressant and can cause
 tremors, weakness, tonic and clonic convulsions, slowed respir-
 ation, and death due to  respiratory paralysis in animals and
 man.  Acute  occupational exposure has caused unconsciousness,
 visual disturbances, an
-------
                                                 .
     and Sons, Hew York.  2,878 pp.

THE MERCK LNDEX.  1976.  9th ed.  Windholz, K., «d.  Merck
     and Co., Rahway, Hew Jtrsey

NATIONAL INSTITUTE FOR OCCUPATIONAL SAFETY AMD HEALTH (NIOSH).
     1984.  Registry of Toxic Effects of Chemical Substances.
     Data Base.  Washington, D.C.  October 19S4

     N.I.  1975.  Dangerous Properties of Industrial Materials.
     4th ed.  Van Nostrand Reinhold Co,< Hew York.   1,258 pages
Dimethylaniline
Page 3
October 1985

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                       DIMt'l'HI
Summary

     in the absence of photolytic degradation, dimethylnitro-
samine is probably persistent in the environment.  Dimethylnitro-
samine is carcinogenic and produces lung, liver, and kidney
tumors in rats and mice and liver tumors in several other animal
species.  It also exhibits transplacental carcinogenicity in
animals and is mutagenic and embryotoxic.  Both acute and chronic
exposure have adverse effects on the liver in humans and experi-
mental.-animals .
CAS Number:  S2-75-I

Chemical Formula:   (CH3)2NNO

IUPAC Mane:  n-Nitrosodimethylamine

Important Synonyms and Trade Names:  n-Methyl-n-nitrosomethanamine,
                                     n,n-d imethylnitrosara ine,
                                     DMN, DMNA, NDMA


Chemical and Physical Properties

Molecular Weight:  74.1

Boiling Pointi  151*C

Specific Gravity:  1.0 at 20*C

Solubility in Hater:  Soluble in all proportions

Solubility in Organicsi  Soluble in organic solvents, lipids

Log Octanol/Water Partition Coefficient:  0.06 to -0.69


Transportandfate

     The aoat probable environmental fate of dimethylnitrosamine
in aqueous solution appears to be slow photolytic degradation.
Furthermore, although supporting data are limited, it has been
speculated that hydrogen bonding of dimethylnitrosamine with
humic acids or coordination with metal cations produces a photo-
labile intermediate and could lead to moderately rapid degrada-
tion in surface waters.  Dimethylnitrosamine has been detected


D imethylni troaamine
Page 1
October 1985



 Preceding page blank                              0*—

-------
 in  the  atmosphere of metropolitan areas and near manufacturing
 facilities  emitting this compound, suggesting  that some atmos-
  fheric  transport can occur.  However/  it  is reported  that photo-
  ytic degradation In air would be rapid,  tilth  a half-life of
 less than 1 hour.  Airborne concentrations in  excess  of a few
 parts per billion appear to be unlikely except near sources
 of  direct emissions.  There is no evidence to  suggest that
 oxidation or hydrolysis are important  environmental fates.

     Dinethylnitrosamine is completely miscible in water and
 is  reported to be highly solvated.  This  information, along
 with limited experimental data* suggtst that volatilization
 from surface waters is probably not an important process.
 Dimethylnitrosaraine has a log octanol/water partition coefficient
 near 0; significant sorption by organic particulates  is therefore
 unlikely.   Experimental evidence confirms this and further
 suggests that sorption by clay particulates in wet soil is
 also unlikely.  Because dlaethylnitrosaaine is completely mis-
 cible in water and has a low log octanol/water partition coeffi-
 cient,  bioaccumulation is probably an  insignificant process.
 Although biodegradation in surface waters does not appear to
 be  an important environmental fate, slow  degradation  of dlmethyl-
 nitrosanine in sewage and soil Is reported to  occur.  Based
 on  this information, it is likely that in the  absence of photo-
 lytic degradation dimethylnitrosamine  would be very persistent
 in  the  environment.


 Health  Effects

     D'imethylnitrosamine is considered to be carcinogenic in
 many experimental animal species by various routes of exposure.
 Dose-response relationships have been  established in  several
 studies.  This compound produces liver, lung,  and kidney tumors
 in  some species of nice and rats after oral and inhalation
 exposure.   Increased incidences of liver  tumors have  also been
 observed in many other aniaal species  after oral administration.
 Inhalation  exposure in rata has produced  tuaors of the ethrotur-
 binals  and  nasal cavity.  Although insufficient epidemiologic
 evidence exists to establish a causative  role  for dimethylnitro-
 samlne  in human carclnogeneais, IARG and  other public health
 organizations recommend that this compound be  regarded as a
 human carcinogen.

     Dimethylnitrosamine is autagenie  in  many  microbial test
 systems with metabolic activation and  in  several other in vivo
 and In  vitro test systems.^ This compound is reported to exhibit
 transplacental carcinogenicity and to  be  eabryotoxlc.  tio terat-
 ogenle effects have been reported.  Acute and  chronic exposure
 of humans and experimental animals to  dlaethylnitrosaaine resulted
 primarily in a variety of hepatotoxic  effects.  In rats, an
 oral LDSQ value of 40 ag/kg and an inhalation  LD-. value of
 37 ag/kg are reported.

 Dimethylnitrosamine
 Page 2
October 1985

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Toxicity to Wildlife and Domestic Animals

     In crayfish exposed to diaethylnitrosanine  in water  foe
6 months, extensive antennal gland degeneration  was observed
at 200,000 ug/liter and hyperplaaia of hepatopancreas  tubular
cells at 100,000 ug/liter.  Rainbow trout  fed dimethylnitrosamine
for 52 weeks showed a dose-related increase in hepatocellular
carcinoma at doses of 200, 400, and 800 Bg/kg,   The weighted
average bioconcentration factor for the edible portion of all
freshwater and estuarine aquatic organisms consumed by Americans
is 0.026.


Regulations and Standards

Ambient Water Quality Criteria  (USEPA):

     Aquatic Life

     Freshwater

     Acute toxicity:  The available data for nitrosamines in
     general indicate that toxic effects occur at concentrations
     as low as 5,3SO ug/liter and would occur at lower concentra-
     tions among species that are nore sensitive than those
     tested.

     Chronic toxicity:  No available data

     Saltwater

     Acute toxielty;  The available data for nitrosamines in
     general indicate that toxic effects occur at concentrations
     as low as 3,300,000 ug/liter and would occur at lower
     concentrations among species that are more  sensitive than
     those tested.

     Chronic toxicity:  Mo available data

     Human Health

     Estimates of the carcinogenic risks associated with lifetime
     exposure to various levels of dlmethylnitrosamine in water
     aret

                                 Concentration

                                 14 ng/liter
                                 1.4 ng/liter
                                 0.14 ng/liter

ACGIR Threshold Limit Value:  Suspected human carcinogen


DinethyInitrosamine
Page 3
October 198S

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REFERENCES

AMERICAN CONFERENCE OF GOVERNMENTAL INDUSTRIAL HYGIENISTS  (ACGIH).
     1980.  Documentation of the Threshold Limit Values.   4th
     ed.  Cincinnati, Ohio.  483 pages

INTERNATIOWAL AGENCY FOR RESEARCI OH CANCER  (IARC).  IARC Monographs
     on the Evaluation of Carcinogenic Risk of Chemicals to
     Humans.  Vol. 17:  Sone N-Nitroso Compounds.  World Health
     Organization, Lyon, France.  Pp. 125-175

NATIONAL INSTITUTE FOR OCCUPATIONAL SAFETY AND HEALTH (NIOSH).
     1984.  Registry of Toxic Effects of Chemical Substances.
     Data Base.  Washington, D.C.  October 1984

SAX, N.I.  1975.  Dangerous Properties of Industrial Materials.
     4th ed.  Van Nostrand Reinhold Co., New York.  1,258 pages

U.S. ENVIRONMENTAL PROTECTION AGENCY (USEPA).  1979.  Water-
     Related Environmental Fate of 129 Priority Pollutants^
     Washington, D.C.  December 1979.  EPA 440/4-79-029

U.S. ENVIRONMENTAL PROTECTION AGENCY (US2PA).  1980.  Aabient
     Water Quality Criteria for Nitrosaaines.  Office of Water
     Regulations and Standards, Criteria and Standards Division,
     Washington, D.C. 'October 1980.  EPA 440/S-80-064
DimethyInitrosamine
Page 4
October 1985
                                                                     f
                                                                   • J

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                        2,4-DIMETHYLPHENOL
Summary
     2,4-Dimethylphenol has been shown to act as a cancer pro-
moter In skin-painting studies, but it has not been tested for
c.arcinogenicity in a complete bioassay.  It is an ATP blocking
agent.  Other Ji.aethylphenols have been shown to cause patholog-
ical changes in the heart, liver, and kidneys.
CAS Numbers  105-67-f

Chemical Formal a j   (CR^^C-H-OB

IUPAC Name:  2,4-Dimethyl-l-hydroxybenzene

Important Synonyms and Trade Harness  m-Xylenol, cresylic acid,
                                     2,4-xylenol


Chemical and Physical Properties

Molecular Weighti  122.2

Boiling Pointi  210*0

Melting Point:  27*C

Specific Gravity*  0.956 at 20°C

Solubility in Waters  17 g/Hter

Solubility in Organicsi  Freely soluble in alcohol, chloroform,
                         ether, and benzene

Log Octanol/Water Partition Coefficient;  2.50

Vapor Pressure:  0.06 mm Hg at 20*C

      10.10
Transport and rate

     Photooxidation is probably the primary mechanism for removal
of 2,4-dimethylphenol in clear, aerated surface waters, although
metal-catalyzed oxidation, sorption, and biodegradation may also
have some effect.  In murky, unaerated water, biodegradation is


2,4-Dimethylphenol
Page 1
October 1985

-------
 probably the primary  fate  of  2, 4-dimethylphenol,  with  absorption
 onto organic materials  also being  somewhat  important.   2, 4 -Dimethyl
 phenol  would be  expected to adsorb onto  organic material  in
 the  soil but becaus*  of its water  solubility  it probably  moves
 readily through  soil.   However,  biodegradation would somewhat
 limit the amount of chemical  able  to  enter  the groundwater.


 Health  affects

     . 2,4-Diraethylphenol has been shown to be  a cancer  promoting
 agent in skin, painting  studies on  rats but  has not been tested
 for  .its total carcinogenic potential.  No studies on the  terato-
 genlcity,  reproductive  toxicity, or mutageniclty  of 2,4-dimethyl-
 phenol  were  found in  the literature reviewed.  At high doses,
 other dinethylphenols have been  shown to cause pathological
 changes in the liver, kidneys, and heart.   2,4-Diaethylphenol
 is known to  be an AT? blocking agent.  Dermal exposure was
 more toxic to rats than oral  dosing.  The reported LD.n values
 for  the rat  were 1,040  rag/kg  (dermal'} and 3,200 ng/kg5ioral) .


 Toxicity to  Wildlife  and Domestic  Animals

     No signs of acute  toxicity  attributable  to 2,4-diraethyl-
 phenol  were  seen in freshwater species exposed to levels  less
 than approximately 2,000 ug/litar.  Chronic toxicity studies
 indicate  that the acute-chronic  ratio is probably between 5
 and  10.  The  bloconcentration factor  in  bluegills exposed to
 2, 4-dimethylphenol for  28  days was 150,  but i half-life in the
 body of less  than one day  suggests that  residues  are probably
 not  a significant hazard for  freshwater  species,  Ho information
 on the  toxicity  of 2,4-dlmethylphenol to other wildlife or
 domestic animals was available in  the literature  reviewed.


 Regulations  and  Standards

Ambient Water Quality Criteria  (USZPA) i

     Aquatic  ti
     The available data are not adequate for establishing cri
     teria.  However, BPA did report the lowest values known
     to causa toxicity In aquatic organisms.

     Freshwater
                          •K
          Acute toxicity:  2,120 ug/liter
          Chronic toxicltyt  No available data
2,4-Dimethylphenol
Page 2
October 198S

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          Acute toxicity:  Mo available data
          Chronic toxicity:  No available data
     Human Health
          Health criterion:  NO available data
          Organoleptic crittcion;  400 ug/liter


REFERENCES

NATIONAL INSTITUTE FOR OCCUPATIONAL SAFETY AND HEALTH (NIOSH).
     1983.  Registry of Toxic Effects of Chemical Substance's.
     Data Base.  Washington, D.C.  October 1983

O.S. ENVIRONMENTAL PROTECTION AGENCY (USEPA).  1179,  Mater-
     Related Environmental Fate of 129 Priority Pollutants.
     Washington, D.C.  Decesber 1979.  EPA 440/4-79-029

O.S. ENVIRONMENTAL PROTECTION AGENCY (DSEPA).  1980.  Ambient
     Water Quality Criteria for 2,4-Diraethylphenol.  office
     of Water Regulations and Standards* Criteria and Standards
     Division, Washington, D.C.'  October 1980.  EPA 440/5-80-023

WEAST, R.E., ed.  1981.  Handbook of Chemistry and Physics.
     62nd ed.  CRC Press, Cleveland, Ohio.  2,332 pages
2,4-Dinethylphenol
Page 3
October 1985
                         9SI

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      n-Dioctyl phthalate  (OOP) was fetotoxic and caused devel-
 opmental abnormalities in one study in cats.  It is a severe
 eye irritant and a mild skin irritant in rabbits.


 CAS Number:  117-84-0

 Chemical Formula:  CgH4(COOCgH17)2

 IOPAC Name;  Di-n-octyl phthallc acid

 Important Synonyms and Trade Names:  o-Benzenedicarboxylic acid,
                                      dioctyl ester, phthalic acid,
                                      dioctyl ester, OOP, octyl
                                      phthalate


 Chemicaland Physical Properties

 Molecular Weight:  391.0

 Boiling Point:  220*C at 5 ma ig

 Melting Point:  -25»C

 Specific Gravity:  0.978

 Solubility in Water:  3 ag/liter at 25*C

 Log Octanol/Water partition Coefficient:  9.2

 Vapor Pressure:  Less than 0.2 at 1SQ*C


 transport andFate

      Although relatively little specific information concerning
 n-dioctyl phthalate (DOP) is available, the environmental trans-
 port and fate of this compound can be largely inferred from data
 for phthalate esters as a group.  DO? probably hydrolyzes in
 surface waters, but at such a slow rate that this process would
 not be significant under most conditions.  Photolysis and oxida-
 tion do not appear to be important environmental fate processes.
 Some atmospheric dispersion of DOP that is vaporized during manu-
 facture, use, or disposal can occur.  However, volatilization
 does not appear to be a significant transport process, especially
 in aquatic systems.


 n-Dioctyl phthalate
 Page 1
 October 1985
Preceding page Wank

-------
     Adsorption  onto  suspended  solids  and particulate natter,
 and  complexation with natural organic  substances are probably
 the  most  important  environmental  transport processes for DOP.
 The  high  log octanol/water partition coefficient for this  com-
 pound  suggests that it would be readily  adsorbed onto particu-
 lates  high  in organic natter.  This contention  is supported  by
 the  fact  that phthalate esters are commonly found in freshwater
 and  saltwater sediment samples.   DOP can be dispersed through
 aquatic and terrestrial systems by complexation with natural
 organic materials.  It readily interacts with the fulvic acid
 present in  huraic substances  in water and soil,  forming a complex
 that is very soluble  in water.

     A variety of unicellular and aultieellular organisms  take
 up and accumulate DOP, and bloaccumulation is considered an
 important fate process.  Biodegradation  is also an  important
 fate process in  aquatic systems and soil.  DOP  is biodegraded
 under  most environmental conditions, and it can be  metabolized
 by multicellular organisms.  It is unlikely that long-term
 bioaceumulation  or biomagnification occurs.

     Analysis based on EPA's Exposure  Analysis  Modeling System
 indicates that chemical and  biochemical  transformation processes
 for  DOP are slow and  that transport processes will  predominate
 both in ecosystems  that have long retention times (ponds,  lakes)
 and  those that have short retention times (rivers).  If the
 input  of DOP remains constant, its concentration is expected
 to increase in aquatic ecosystems.  If input stops, the DOP
 present is expected to persist for an  undetermined  length  of
 time.  The oceans are the ultimate sink  for DOP introduced
 into unimpeded rivers.


 Health Effects

     There is no evidence to suggest that DOP is carcinogenic
 or mutagenic.  Fetotoxicity and developmental abnormalities
 were observed in the offspring of rats administered 5 g/kg
 intraperitoneal  injections on days 5 to  15 of gestation.   Ho
 other  evidence for reproductive or teratogenic  effects has
 been reported.

     very little information exists concerning  the  chronic
 and  acute toxicity of DOP.  A chronic  LD,Q value of 1.3 mg/kg
 was  determined for mice receiving intrapcritoneal injections
 of DOP S days/week for 10 weeks.  DOP  has a relatively low
 acute  toxicity in mice with reported oral and intraperitoneal
LD5Q values of 6.5 and 65 g/kg, respectively.   This chemical
 is I severe eye  irritant and a mild skin irritant in rabbits.
n-Dioctyl phthalate
Page 2
October 1985

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     Seven to tight-day LC»Q values for freshwater species
range froa 190 to 42,000 ug7liter.  A 26-day LC-0 value of
149,200 pg/littr was reported for rainbow trout.

     freshwater snails and mosquito larvae were found to have
bioconcentration factors of 13,600 and 9,400, respectively,
in model ecosystems.  The.bioconcentration factor for a fresh-
water alga is 28,500.


Regulations and Standards

Ambient Hater Quality Criteria  (USEPA):

     The available data are not adequate for establishing criteria,


REFERENCES

NATIONAL INSTITUTE FOR OCCUPATIONAL SAFETY AND HEALTH {NIOSH}.
     1984.  Registry of Toxic Effects of Chemical Substances.
     Data Base.  Washington, D.C.  July 1984

NATIONAL TOXICOLOGY PROGRAM AND THE INTERAGENCY REGULATORY
     LIAISON GROUP.  1982.  The Conference on Phthalates.
     Environ. Health Perspeet. 45J1-153

U.S. ENVIRONMENTAL PROTECTION AGENCY (USEPA).  1979.  Water-
     Related Environmental Fate of 129 Priority Pollutants.
     Washington, D.C.  December 1979.  EPA 440/4-79-029

U.S. ENVIRONMENTAL PROTECTION AGENCY (USEPA).  1980.  Ambient
     Hater Quality Criteria for Phthalatt Esters.  Office of
     Hater Regulations and Standards, Criteria and Standards
     Division, Washington, D.C.  October 1980.  EPA 440/5-80-067
n-Dioctyl phthalate
Page 3
October 1985

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-------
                            1,4-DIOXANE
 Summary
      1,4-Dioxane caused tumors of the liver and nasal cavity
 tn rats and liver and gall bladder tumors in guinea pigs,
 IARC has classified dioxane as a potential human carcinogen.
 Dioxane irritates the eyes and mucous membranes, and inhalation
 of high concentrations causes liver and kidney damage and edema
 of the lungs and brain.
 CAS Number:  123-91-1
 Chemical Formula:  0(Ca2-CH2)20
 IUPAC Kane:  1,4-Dioxane
 Important Synonyms and Trade Mames:  p-Dioxane, glyeol ethylene
                                      etheri 1,4-diethylenedioxya
 Chemical and Physical Properties
 Molecular Height:  88.20
 Boiling Points  101*C
 Melting Point:  10*C
 Specific Gravity:  1.033 at 2Q*C
 Solubility in Water:  Soluble in water
 Solubility in Organics:  Soluble in organic solvents
 Log Octanol/Water Partition Coefficient:  -0.42
 Vapor Pressure!  30 BIB Eg at 20*C
 Vapor Density:  3.03
 Flash Point:  S*C to 18*C

 Transport and Fate
      The limited information found on the transport and fate
 of 1,4-dioxane in the environment suggests that this compound
 is rather nonreactlve.  Dioxine would be expected to evaporate
 slowly; but once in the atmosphere, it should form explosive

 1,4-Dioxane
 Page 1
 October 198S
                                                 C Clement
Preceding page blank

-------
peroxides.  It  I* metabolized by animals to beta-hydroxyethoxy-
acetic acid and may b€ biodegraded in a similar fashion by
microorganisms.  However, no data on biodegradatlon were available


Health Effects

     1,4-Dioxane has produced malignant tumors of the liver
and nasal cavity in rats after chronic exposure and tumors
of the liver and gall bladder in guinea pigs after long-term
oral administration.  In a two-stage carcinogenesis study per-
formed on Swiss-Webster mice, it was also determined that dioxane
is a promoter.  However, tumors did not develop when rats were
exposed to 1,4-dioxane by inhalation.  On the basis of the
animal studies, it has been concluded that 1,4-dioxane is a
potential human carcinogen {IARC 1976).  Dioxane has been found
to damage DNA, and the results of an in vivo DMA synthesis
test were positive.  The evidence on the teratogenic potential
of dioxane is inconclusive.

     Dioxane reportedly irritates the eyes, nose,.and throat
of humans exposed to concentrations of 1,080 mg/ra  or more
for 15 minutes.  Prolonged exposure to concentrations above
1,690 ag/m  has caused death, with signs of kidney damage,
anemia, and liver necrosis.

     In inhalation studies, nice, rabbits, rats, and auinea
pigs were exposed to concentrations above 14,400 mg/ra .  lyper-
emia and edema of the lungs and brain, in addition to liver
and kidney damage, were reported.  Experiments with animals
indicate that dioxane is not appreciably irritating to intact
skin, but it is readily absorbed and causes defatting of the
skin layers.  The acute U5SQ values are 5*7 g/kg body weight
for mice, 5.2 g/kg body weight for rats, and 3.9 g/kg body
weight for guinea pigs.  The dermal LD.Q for rabbits is 7.6 g/kg.
Several studies indicate that dioxane may act synergistieally
with other chemicals.


Toxicity to Wildlife and Domestic Animals

     The data on the toxicity of 1,4-dioxane to wildlife and
doaestie animals are limited.  The 96-hour X.C.. for the bluegill
is more than 10,000 mg/liter, and it is f,7003If/liter for
the tidewater silverside, a saltwater fish.  The threshold
for inhibition of cell division of the alga Microcystis aeruginosa
is 575 rag/liter; the threshold for inhibition of cell division
in the bacteriun fseudomonas putIda is 2,700 ag/liter.
1,4-Dioxane
fage 2
October 1985

-------
Regulation^and Standards

NIOSH Recommended standard:  4 mg/m3/30 min Ceiling Limit

03.HA Standard  (skin):  360 rag/™3 TWA.

ACGIH Threshold Limit Value;  90 mg/m3 TWA


REFERENCES

AMERICAN CONFERENCE OF GOVERNMENTAL INDUSTRIAL HYGIENISTS {ACGIH),
     1980.  Documentation of the Threshold Limit Values.  4th
     ed.  Cincinnati, Ohio.  488 pages

DOULL, J., KLAASSEN, C.D., and AMDOR, M.O., eds.  1980.  Casarett
     and Doull's Toxicology:  The Basic Science of Poisons.
     2nd ed.  Mac™illan Publishing Co., New York.  778 pages

INTERNATIONAL AGENCY FOR RESEARCH ON CANCER (IARC).  1976.
     IARC Monographs on the Evaluation of Carcinogenic Risk
     of Chemicals to Nan.  Vol. 11:  Cadmium,  Nickel, Some
     Epoxides, Miscellaneous Industrial Chemicals, and General
     Considerations on Volatile Anaesthetics.   World Health
     Organization, Lyon, France.  Pp. 247*256

LYMAN, W.J., RSEHL, W.P., and ROSENBLATT, D.H.  1982.  Handbook
     of Chemical Property Estimation Methods:   Environmental
     Behavior of Organic Compounds.  McGraw-Hill Book Co.,
     New York

THE MERCK INDEX.  1976.  9th ed.  Windholz, M., «d.  Merck
     and Co., Rahway, New Jersey

NATIONAL CANCER INSTITUTE (NCI).  1978.  Bioassay of 1,4-Dioxane
     for Possible Carcinogenicity.  {CAS Ho. 123-91-1)  NCI
     Carcinogenesis Technical Report Series No. 80.  Washington,
     D.C.  DEEW Publication NO. (NIB) 78-1330

NATIONAL INSTITUTE FOR OCCUPATIONAL SAFETY AND HEALTH (NIOSH).
     1977.  'Criteria for a Recommended Standard—Occupational
     Exposure to Dioxane.  Washington, D.C.  DHEW Publication
     No. (NIOSI) 77-22S

NATIONAL INSTITOTS FOR OCCUPATIONAL SAFETY AND HEALTH (NIOSH).
     1984*  Registry of Toxic Effects of Chemical Substances.
     Data Base.  Washington, D.C.  October 1984

SAX, N.I.  1975.  Dangerous Properties of Industrial Materials.
     4th ed.  Van Nostrand Reinhold Co., New York.  1,258 pages
1,4-Dioxane
Page 3
October 1985

-------
VERSCHUEREN, R.  19??.  Handbook of invironaental Data on Organic
     Chemicals.  Van Nostrand Reinhold Co., New Yoclc.   659 pages

WEAST, R.E., «d.  1981.  Handbook of Chemistry and Physics.
     62nd ed.  CHC Preas, Cleveland/ Ohio.   2,332 pages
1,4-Dioxane
Page 4
October 19S5

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                          DIPHSNYLSTHAME


Summary

     Diphenylethane was shown to be moderately toxic In nice
after acute exposure.


CAS Number*  103-29-7

Chemical Formulas   (CgHgJCHjCHj (CgSg)

IOPAC Name:  I,2-Diphenylethane

Important Synonyms and Trade Names:  Bibenzyl, dibenzyl, and
                                     1,2-diphenylethane


Chemical and Physical Properties

Molecular Weight:  182

Boiling Point:  284*C

Melting Point:  52*C

Specific Gravityz  0.978

Solubility in Water:  Insoluble in water

Solubility in Organics:  Soluble in alcohol, chloroform, ether
                         and carbon disulfide

Log Octanol/Water Partition Coefficient:   4.9 (calculated)


Transport and Fate
  jf
     No information on the transport and fate of diphenylethane
was available in the sources reviewed.  Based on its log octan-
ol/water partition coefficient, diphenylethane is probably
adsorbed by the organies in soil and sediment.  Its ultimate
fate in the environment is likely to be either photooxidation
or biodegradation by soil microbes,


Health effects

     The available data on the toxicity of diphenylethane was
extremely limited.  The intrap*ritoneal and intravenous LD.Q
values for mice, which are 2,500 «g/kg and 78 mgAg, respective
ly, were the only values reported.

Diphenylethane
Page 1
October 1985

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Toxicity to Wildlife and Pomestic Animals

     Ho information on the toxicity of diphenylethane to wildlife
and domestic animals was found in the sources reviewed.


REFERENCES

LYMAN, W.J., REEHL, W.F., and ROSENBLATT, D.H.  1982.  Handbook
     of Chemical Property Estimation Methods:  Environmental
     Behavior of Organic Compounds.  McGraw-Hill Book Co.,
     Sew York

THE MERCK INDEX.  1976.  9th ed.  Windholz,  M., «d.  Merck
     and Co., Rahway/ New Jersey

NATIONAL INSTITUTE FOR OCCUPATIONAL SAFETY AND HEALTH (NIOSH).
     1984*  Registry of Toxic Effects of Chemical Substance's.
     Data Base.  Washington, D.C.  October 1984

SAX, N.I.  1975.  Dangerous Properties of Industrial Materials.
     4th ed.  Van Nostrand Reinhold Co., New York.  1,253 pages

VSRSCHUERENf K.  1977.  Handbook of Environmental Data on Organic
    'Chemicals.  Van Nostrand Reinhold Co.,  New York,  659  pages

WEAST, R.E., ed.  1981.  Handbook of Chemistry and Physics.
     62nd ed.  CRC Press, Cleveland, Ohio.  2,332 pages
Diphenylethane
Page 2
October 1985
                                                                 - Jf

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                              ENDRIN
Summary
     Endrin  is a cyclodiene insecticide that is an isomer of
dieldrin.  It is probably retained in soils and sediments and
is persistent in the environment.  It is strongly bioaccunualted
by aquatic organisms.  Endrin is highly toxic to mammals, aquatic
organisms, and terrestrial wildlife after acute exposure.  It
has not been shown to be carcinogenic or mutagenic, but it
is a potent  teratogen and reproductive toxin.
CAS Numberi  72-20-8

Chemical Formulas  Cj-HgCl^O

IUPAC Name:  l,2»3,4,10,10-Hexachloro-6,7-epoxy-l,4,4a,5,6,7,8,8a
             octahydro-endo-1,4:5,8-dimethanonaphthalene

Important Synonyms and Trade Naaest  indrex, hexadrin, mendrln


Chemical and Physical Properties

Molecular Weights  380.9

Melting Points  Decomposes at 235*C

Specific Gravity!  1.65 at 2S*C

Solubility in Waters  250 ug/liter at 25«C

Solubility in Organic*!  Soluble in acetone, benzene, carbon
                         tetrachloride, hexane, and xylene

tog Octanol/Water Partition Coefficients  5.6

Vapor Pressures  2.7 i Id*"7 an Hg at 25'C


Transport and Fate

     Endrin Im quite persistent in the environment.  Volatiliza-
tion froa soil surfaces and probably from surface water is
an important transport process  (Nash 1983).  Subsequent photol-
ysis to delta-keto endrin and endrin aldehyde are apparently
important fate processes.  No information on the ability of


Bndrin
Page 1
October 1985
                                                 G



                                 2C.3

-------
cndrin  to  adsorb  to  soils  and  sediments  was  found  in  the  liter-
ature reviewed, but  the physical properties  of  the  chemical
suggest  that  sorption would  be  an  important  fate process.
Endrin  is  readily bioeoncentrated  by aquatic organisms, with
concentration factors of 10  to 10 .  liotransformation and
biodegradation nay also be important fate processes for endrin.


Health Effects

    ..Endrin has not  been shown  to  b« carcinogenic or  taut age nic.
However, it is a  potent reproductive toxin and  teratogen  in
experimental  animals.  Reproductive effects  included  fetal
mortality  and growth retardation,  while  teratogenic effects
included cleft palate, open  eye, clubbed foot,  meningoencephales,
and fused  ribs.   Chronic exposure  to Ion levels of  endrin pri-
marily results in nervous  system damage  but  also has  adverse
effects on the heart, lungs, liver, and  kidneys.  The acute
toxicity of endrin is due  to its effects on  the central nervous
system.  The  acute oral and dermal LD-.  values  for  endrin to
the rat were  both approximately IS mg/Rg.


Toxicity to Wildlife and Domestic  Animals

     Endrin is very  toxic  to aquatic organisms.  Freshwater
fish were generally  more sensitive than  invertebrates, with
species mean  acute values  ranging  froa 0.15  to  2.1  ng/liter.
LC5Q values for saltwater  organisms ranged from 0.93? to
1412 tig/liter.  Final acute values for freshwater and saltwater
species were  0.18 pg/liter and  0.037 pg/liter,  respectively.
An acute-chronic  ratio of  4.0 was  determined from chronic tests
on freshwater  and saltwater species.  Therefore, the  freshwater
final chronic  value  was calculated to be 0.045  ug/liter and the
saltwater  final chronic value was  determined to be  0.0093 yg/liter,

     Sndrin is acutely toxic to terrestrial  wildlife  and domestic
animals and has been used  as a  rodenticide and  an avlcide.  It
can also cause central nervous  system effects and reproductive
disorders following  chronic exposure.  Sublethal effects observed
in animals exposed to endrin Include abnormal behavior, increased
postnatal mortality, and increased fetal death.


Regula t i ona and 3tandards

Ambient Water  Quality Criteria  (USEPA)i
Endrin
Page 2
October 1985

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     Freshwater
          Acute  toxicity:  0.18 Mg/liter
          Chcontc toxicity:  0.0023 ug/llter

     Saltwater

          Acute  toxicity:  0.03? Mg/liter
          Chronic toxicity:  0.0023 ug/liter

     Human Health

     Criteriont  1.0 pg/liter

Primary Drinking Water Standard:  1.0 us/liter

OSHA Standard:   100 pg/m3 TWA


REFERENCES

JAGER, K.W.  I9?o.  Aldrin, Dieldrin, Endrin, and Ttlodin.
     Elsevier Publishing Co., New York.  234 pages

NASH, R.G.  19S3.  Comparative volatilization and dissipation
     rates of several pesticides from soil.  J. Agric. Food
     Chem. 31:310-217

NATIONAL INSTITUTE FOR OCCUPATIONAL SAFETY AND HEALTH (NIOSH).
     1983.  Registry of Toxic Effects of Chemical Substances,
     Data Base.  Washington, D.C.  October 1983

U.S. ENVIRONMENTAL PROTECTION AGENCY (USEPA).  1979.  Water-
     Related Environmental Fate of 129 Priority Pollutants.
     Washington, D.C.  December 1979.  EPA 440/4-79-029

U.S. ENVIRONMENTAL PROTECTION AGENCY (USZPA).  1980.  Ambient
     water Quality Criteria for Chlorinated Endrin.  Office
     of Water Regulations and Standards, Criteria and Standards
     Division, Washington, D.C.'  October 1980.  EPA 440/5-80-028

VERSCHOBREN, K.  1977.  Handbook of Environmental Data on Organic
    'Chemicals.  Van Nostrand Reinhold Co., New York.  659 pages

WEAST, R.B.i ed.  1981.  Handbook of Chemistry and Physics.
     62nd ed.  CRC Press, Cleveland, Ohio.  2,332 pages
Endrin
Page 3
October 1965

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                              ETHANOL
 Summary
      Ethanol is probably responsible foe some of the increased
 risk of cancer associated with the consumption of alcoholic
 beverages, and it has been found to be mutagenic using several
 assays.  Alcohol consumption has also been associated with
 a number of teratogenic and reproductive effects and with liver
 cirrhosis and irritation of the mucous membranes.
 CAS Number:  (4-17-5
 Chemical Formula;  CjHjOH
 IDPAC Name:  Ethanol
 Important Synonyms and Trade Names:  Ethyl alcohol, grain alcohol

 Ch«mical_and_ Physical Properties
 Molecular Weight:  46
 Boiling Point:  78.4*C
 Melting Points  -114. 1*C
 Specific Gravity;  0.789 at 20*C
 Solubility in Haters  Miicible in water
 Solubility in Organics:  Soluble in alcohol, benzene, and ether
 Log Oetanol/Water Partition Coefficient:  -0.31
 Vapor Pressure:  44 ma Hg at 20*C
 Vapor Density:  1.59
 Flash Point:  14*C (closed cup)

 Transport and Fate
      No information on the transport and fate of ethanol was
 found in the sources reviewed.  However* based on the general
 reactions of alcohols and the specific chemical and physical
 properties of the material, likely transport and fate processes
 can be determined.

 Ethanol
 Page 1
 October 1985
Preceding page blank              ~, ~

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     Alcohols are very soluble  in water and therefore probably
are not very volatile.  Some evaporation is likely to occur,
however, especially for a compound such as ethanol with a  rela-
tively high vapor pressure.  Oxidation is probably an important
fate process in both surface water and the atmosphere.  In
soil, ethanol is probably biodegraded by soil microorganisms.


Health Effects

     The consumption of alcoholic beverages has been associated
with the development in humans  of cancer of the esophagus,
stomach, colon, and rectum.  Excessive consumption of alcohol
also appears to act synergistically with smoking to increase
the risk of cancer of the mouth, larynx, esophagus, and respir-
atory tract.  Alcohol abuse causes liver cirrhosis, which aay
in turn lead to hepatoaas.  Although it appears that at least
some of the cancers associated  with alcohol consumption aay be
due to constituents other than  ethanol, ethanol is probably re-
sponsible for some of the increased risk of cancer.  Ethanol was
found to be mutagenic in several genotoxicity assays.  A number
of reproductive and teratogenie effects are associated with
alcohol consumption.  These include growth deficiencies, delayed
motor development, cardiac anomalies, and mental deficiency.
Peterson et al. (1981) gave intraperitoneal doses of 6,000 mg/kg
daily to pregnant mice on days  6 to 17 of gestation and noted
increased resorption and an increase in the incidence of cleft
palates.

     Excessive ethanol consumption causes liver cell damage
and cirrhosis of the liver, as  well as the well-known behavioral
effects.  Ethanol is also an irritant to the mucous membranes.
The oral LD5Q in rats was reported to be 7,060 ag/kg.


Toxicity to Wildlife and Domestic Animals

     The 24-hour LDQ and LDlftfl  values for the creek chub were
7,000 and 9,000 ing/liter of ethanol, respectively.  The algae
Chlorella pyrenoidosa had an liC5Q of 27,000 «g/liter.

     No information on the toxic effects of distilled ethanol
to terrestrial wildlife or domestic animals was found in the
literature reviewed.  However,  both terrestrial wildlife and
domestic animals have been known to become intoxicated after
the consumption of fermented fruit or grain.
Ethanol
Page 2
October 19SS
                                                                   J

-------
{teg u A a v*Oftb ar>u a *«»<«»•*..».a

OSHA Standard  (air)t  1,900 mg/m3 TWA

ACGIH Threshold Limit Value:  1,900 mg/ra3 TWA
REFERENCES

AMERICAN CONFERENCE OF GOVERNMENTAL INDUSTRIAL HYGIENISTS  (ACGIH),
     1980.  Documentation of the Threshold Limit Values.  4th
     ed.  Cincinnati, Ohio.  488 pages

AMERICAN INDUSTRIAL HYGIENE ASSOCIATION  (AIHA).  1978.  Hygienic
     Guide Secies.  Ethanol.  AIHA, Akron, Ohio

LYMAN, W.J., RtEBL, W.F., and ROSENBLATT, D.H.  1982.  Handbook
     of Chemical Property Estimation Methods:  Environmental
     Behavior of Organic Compounds.  McGraw-Hill Book Co.,
     New York

THE MERCK INDEX.  1976.  9th ed.  Windholz, M., ed.  Merck
     and Co.t Rahway, New Jersey

NATIONAL INSTITUTE FOR OCCUPATIONAL SAFETY AND 1EALT1  (NIOSI).
     1984.  Registry of Toiie Effects of Chemical Substances.
     Data Base.  Washington, D.C.  October 1984

NATIONAL RESEARCH COUNCIL IMSCJ.  1982.  Diet, Nutrition, and
     Cancer.  Committee on Diet, Nutrition, and Cancer, Assembly
     of Life Science, NRC«  National Academy Press, Washington,
     D.C.

PETERSON, K.L., HENINGER, R.W., and SEEGMILLER, R.E.  1981.
     Fetotoxicity following chronic prenatal treatment of mice
     with tobacco smoke and ethanol.  Bull. Environ. Contain,
     Toxicol. 26t813-8l9

SAX, N.I.  1975.  Dangerous Properties of Industrial Materials.
     4th ed.  Van Nostrand Reinhold Co., New fork.  1,258 pages

VERSCHOEREN, X.  1977.  Handbook of Environmental Data on Organic
    "Chemicals.  Van Nostrand Reinhold Co., New York.  €59 pages

WEAST, R.E., ed.  1981.  Handbook of Chemistry and Physics.
     62nd ed.  CSC Press, Cleveland, Ohio.  2,332 pages
Ethanol
page 3
October 1985

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-------
                            2THANOLAMINE
  Summary
      Ethanolamine  caused  liver  and  kidney changes when admin-
  istered  ofally  to  cats  and  liver, lung,  and  kidney lesions
  when administered  by inhalation to  mice,  rats,  rabbits, and
  guinea pigs.  In humans,  it has an  irritant  and necrotic effect
  on  the skin  and mucous  membranes, and  it is  a strong  eye irritant.
  CAS Number:   141-43*5
  Chemical Formula:   NH_CH.CH2OH
  IUPAC Name;   Ethanolamine
  Important Synonyms and  Trade Names:  Nonoethanolamine, 2-arainoethano
                                      8-aaino ethyl alcohol, ethylol-
                                      amine,  0-hydroxyethylamine,  HEA
  Chemical and  Physical Properties
  Molecular Weight:   61.1
  Boiling  Points  17Q«C
  Melting  Point:  10.3«C
  Specific Gravity:   1.018  at 20*C
  Solubility in Water:  Completely miscible in water
  Solubility in Organics:   Soluble in alcohol  and chloroform
  Log Octanol/Water  Partition Coefficient:   -1.8  (calculated)
  Vapor Pressure:  0.4 na If  at 20*C
  Vapor Density:  2.1
  Flash Point!  95*C (closed  cup)

  Transport and Pate
  •^M^a^^^^^^^^MM^^^^M^^^^^^^^^MM^aa     ^
      No  specific information on the transport and fate of ethanol-
  amine was found in the  literature reviewed.   The high water
  solubility and  low vapor  pressure suggest that  ethanolamine
  will not volatilize and will tend to move readily with ground-

  Ethanolamine
  Page 1
  October  1985
                                                  ^JCiemerte Ammocmtmm
Preceding page blank

-------
 or  surface  water  flow.  It  is  a  relatively  strong  base  and
 will  therefore disassociate  in acidic media,
Health  Sffeeta

     No information on  the carcinogenicity, mutagenicity, repro-
ductive toxicity, or  teratogenicity of ethanolamine was  found
in  the  sources  reviewed.  Subchronic  (90 day) administration
of  oral doses of 320  rag/kg/day  in  feed had no effect on  rats,
but doses of 140 ag/kg  caused increased liver and kidney weights,
and doses of 1,280 mg/kg/day caused histopathological changes
in  these organs and some deaths.   Inhalation exposure of rats,
nice, rabbits,  and guinea pigs  to  the high concentrations of
a vapor or a mist produced hepatic, pulmonary, and renal lesions.
Exposure to 15 ng/ra   of ethanolamine for 90 days caused  skin
irritation, a slight  weight loss,  and slight apathy in dogs.

     Ethanolamine has an irritant  and necrotic effect on the
skin and mucous membranes.  It  is  only slightly less irritating
to  the  eye than ammonia and causes redness and swelling  when
applied to the  skin.  The dermal LD_fl in eats of 1,500 ag/kg
is  lower than the oral  LD5Q in  rats'of 2,100 *f/*g.


Toxicity to Wildlife  and Domestic  Animals

     The toxicity of  ethanolamine  to aquatic organisms is de-
pendent on the pH of  the system.   Goldfish exposed to ethanol-
amine at a pH of 10.1 had 24- and  96-hour LC-fl values of 190
and 170 ag/liter, respectively.  Goldfish exposed for 24 hours
at  a pH of 7 had a reported LC.. of greater than 5,000 ag/liter.
ha  aost natural waters  have a pa less than 7, ethanolamine
is  not  likely to be an  important aquatic toxin.

     No information on  the toxicity of ethanolamine to terres-
trial wildlife or domestic animals was available in the  liter-
ature reviewed.


Regulations and Standards

OSHA Standard (air)s  8 mg/m3 TWA

ACGIH Threshold Limit values:   8 mg/m3. TWA
                        ^       15  mg/ra  STEL


REFERENCES

AMERICAN CONFERENCE OF GOVERNMENTAL INDUSTRIAL HYGIENISTS (ACGIH)
     1980.  Documentation of the Threshold Limit Values.  4th
     ed.  Cincinnati, Ohio.  488 pages

Ethanolamine
Page 2
October  1985

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AMERICAN INDUSTRIAL HYGIENE ASSOCIATION (AIHA).   1978.  Hygienic
     Guide Series.  Ethanolamines.  AIHA,  Akron, Ohio

LYMAN, W.J., RZEHL, W.F., and ROSENBLATT,  D.H.  1982.  Handbook
     of Chemical Property Estimation Methods:  Environmental
     Behavior of Organic Compounds.  McGraw-Hill Book Co./
     Hew York

THE MERCK INDEX.  1976.  9th ed.  Windholz, M.,  ed.  Merck
     and Co., Rahway, Hew Jersey

NATIONAL INSTITUTE FOR OCCUPATIONAL SAFETY AND HEALTH (NIOSH).
     1984.  Registry of Toxic Effects of Chemical Substances.
     Data Base.  Washington, D.C.  July 1984

SAX, N.I.  1975.  Dangerous Properties of  Industrial Materials.
     4th ed.  van Nostrand Reinhold Co., New York.  1,258 pages

VERSCHUEREK, K.  1977.  Handbook of Environmental Data on Organic
     Chemicals,  van Nostrand Reinhold Co., New York.  €59 pages

WEASTi R.E., ed.  1981.  Handbook of Chemistry and Physics.
     62nd ed.  CRC Press, Cleveland, Ohio.  2,332 pages
Ethanolaaine
Page 3
October 1985
                                                  [d

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                          ETHYL ACETATE


Summary

     Inhalation exposure to high levels of ethyl acetate caused
pulmonary edema; hemorrhage of the respiratory tract; leukocy-
tosis; and fatty degeneration of various organs, including
the liver.  Ethyl acetate is a mild irritant of the eyes and
aucous membranes.


CAS number:  141-78-6

Chemical Formula!  CH.COOC^Be

IUPAC Name:  Ethyl acetate

Important Synonyms and Trade Names:  Acetic ether, ethyl acetic
                                     acid, ethyl ethanoate,
                                     vinegar naphtha


Chemical and Physical Properties

Molecular Weight:  88.1

Boiling Joints  77*C

Melting Foint:  -83*C

Specific Gravity:  0.902 at 20*C

Solubility in Water:  79,000 mg/liter at 20»C

Solubility in Organicsi  Soluble in alcohol, chloroform, and ether

Log Oc t an o I/Water partition Coefficient,!  1.0 (calculated)

Vapor Pressures  76 am Eg at 20*C

Flash points  -4»C


Transport and Pate

     No information on the transport and fate of ethyl acetate
was found in the literature reviewed.  The chemical has a rela-
tively high vapor pressure, but volatilization will be somewhat
limited by its high water solubility.  Esters usually undergo
•low hydrolysis in acidic aedia, and hydrolysis to acetic acid
and ethanol is probably a major fate pathway for ethyl acetate.


Ethyl acetate
Page 1
October .1985
Preceding page blank

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Reduction to fora 2 molecules of ethanol could also be impor-
tant in a reducing environment.


Health effects

     Ethyl acetate was not found to be carcinogenic in a very
United mouse lung tumor bioassay  (Stoner et al. 1973).  Mo
information on its autagenicity or reproductive toiicity was
found in the sources reviewed.

     Animals exposed by inhalation-to high concentrations of
the vapor (greater than 6,000 ag/a ) exhibited pulmonary edema,
hemorrhage of the respiratory tract, leukocytosis, and fatty
degeneration of various organs, including the liver.  Humans
exposed to 1*400 mg/m  noted mild  irritation of the nose, eyes,
and throat.  The acute oral LD.n of ethyl acetate in rats is
6,100 atg/kg.                  3U


Toxicity to Wildlife and Domestic Animals

     No information on the toxicity of ethyl acetate to wildlife
or domestic animals was available  in the sources reviewed.


Regulations and 51andards

OSHA Standard (air):  1,400 mg/m3 TWA

ACGIH Threshold Liait Value:  1,400 mg/m3 TWA


REFERENCES  '

AMERICAN CONFERENCE Of GOVERNMENTAL INDUSTRIAL HYGIENISTS (ACGIH).
     19SO.  Documentation of the Threshold Limit Values.  4th
     ed.  Cincinnati, Ohio.  488 pages

AMERICAN INDUSTRIAL BYGIENE ASSOCIATION (AIHA).  1978.  Hygienic
     Guide series.  Ethyl Acetate.  AISA, Akron, Ohio

THE MERCK INDEX.  1976.  9th ed.  Windhola, M., ed.  Merck
     and Co., Rahway, New Jersey

NATIONAL INSTITUTE FOR OCCUPATIONAL SAFETY AND HEALTH  (NIOSH).
     1984.  Registry of Toxic Effects of Chemical Substances.
     Data Base.  Washington, D.C.  October 1984

SAX, N.I.  197S.  Dangerous Properties of Industrial Materials.
     4th ed.  Van Hostrand Reinhold Co., New York.  1,258 pages
Ethyl acetate
fage 2
October 1985
                                                                    J

-------
 STONER,  C.D.,  SB1MXIN, N.B., KNIAZEFP, A.J., WEISBORGER, J.R.,
     WZISBURGER, E.K., and GORI, 
-------

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                             ETHYLBSNZEN1
  Summary
       There Is some evidence suggesting that ethylbenzene causes
          reproductive effects In animals.  Oral and inhalation
  exposure caused minor liver and Kidney changes in fats.  Ithvl-
  benzene is a akin and eye irritant.
  CAS" 'Number:  100*41-4
  Chemical Formula;  CeH-C.,He
                      o 5 2 5
  IUPAC Ham* s  Ethylbenzene
  Inportant Synonyms and Trade Names i  Phenylethane, ES, ethylbenzol
  Chemical and Physical Properties
  Molecular Weight:  106.2
  Boilinf Point*  136. 2*C
  Melting Pointi  -95*C
  Specific Gravity}  0.867 at 20*C  (liquid)
  Solubility in Water:  161 ng/liter at 2S*C
  Solubility in Organics:  Frtely soluble in organic solvents
  Log octanol/water partition Coefficients  3.15
  Vapor Pressure:  7 aa Hf at 20 *C
  Vapor Oensityt  3.16
  Henry's Lav Constant!  6.44 atra. m /mole
  Flash point i  17.2*C
  Transport and Fate
                          \
       Only limited data are available on the transport and fate
  of ethylbenzene.  Volatilization is probably the major route
  of elimination Iron surface water.  Subsequent atmospheric
  reactions , especially photooxidation, are responsible for its
  Ethylbenzene
  Page  1
  October 1985
Preceding page blank

-------
fate,  However,  its high log octanol/water partition coefficient
suggests that a  significant amount of ethylbenzene  may be
adsorbed by organic aaterial in the sediment.  Some soil bacteria
are capable of using ethylbenzene as a source of carbon.  How-
ever, the relative importance off this potential route of ethyl-
benzene elimination has not been determined.


Health Effects

   .'* Ethylbenzene has been selected by the National Toxicology
Program to be tested for possible carcinogenic!ty, although
negative results were obtained in mutageniclty assays in Salmonella
typhimuciua and  Saceharomyces eer e vi s i ae.  There is recent
animal evidence  that ethylbenzene causes adverse reproductive
effects.  Ethylbenzene is a skin irritant, and its vapor is
irritating to the eyes at a concentration of 200 ppn (870 mg/m3)
and above.  When experimental animals were exposed to ethylbenzene
by inhalation* 7 hours/day for 6 months, adverse effects were
produced at concentrations of €00 ppn (2,610 mg/m ) and above,
but not at 400 ppm (1,740 mg/m ).  At €00 ppm rats and guinea
pigs showed slight changes in liver and kidney weights, monkeys
had slight changes in liver weight, and monkeys and rabbits
experienced histopathologic changes in the testes.  similar
effects on the liver and kidney were observed in rats fed ethyl-
benzene at 408 and €80 rag/kg/day for € months.


Toxicity to Wildlife and Domestic Animals

     Ethylbenzene was acutely toiic to freshwater species at
level's greater than 32 mg/liter.  Ho chronic toxicity was re-
ported, but the highest test dose (440 pg/liter) was only one-
hundredth of the 96-hour LC«0 for the particular species being
tested.  Ho studies on the Bloaccumulation of ethylbenzene
were reported in the information reviewed, but i bioconcentration
factor of 9S was calculated using) the log octanol/wster partition
coefficient.  Ho inforaation on the toxicity of ethylbenzene
to domestic animals and terrestrial wildlife was found In the
sources reviewed.


Regulations and Standards

Ambient Water Quality Criteria (DSEPA)i

     Aquatic Life

     The available data are not adequate for establishing final
     criteria.  However, EPA did report the lowest values known
     to have toxic effects in aquatic organisms.
Ethylbenzene
Page 2
October 1985
                                                                     /

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     Freshwater
         Acute  toxicity:  32,000 yg/liter
         Chronic texieity:  No available data

      Saltwater

         Acute  toxicity:  430 pg/liter
         Chronic toxicity:  No available data


      Human Health

      Criterion:  1.4 ag/liter

OSHA  Standard  (skin):  435 mg/m3 TWA

ACGIH Threshold Limit Values:  435 ag/m| TWA
                               545 mg/aj STEL


REFERENCES              »

AMERICAN CONFERENCE OF GOVERNMENTAL INDUSTRIAL HYGIENISTS (ACGIH).
      1980.  Documentation of the Threshold Limit Values. ' 4th
      ed.  Cincinnati, Ohio.  488 pages

AMERICAN INDUSTRIAL HYGIENE ASSOCIATION (AIHA).  1978.  Hygienic
      Guide Series.  Ethyl Benzene.  AIHA, Akron, Ohio

NATIONAL INSTITUTE FOR OCCUPATIONAL SAFETY AND HEALTH (NIOSH).
      1983.  Registry of Toxic Effects" of Chemical Substances.
      Data Base.  Washington, D.C.  October 1983

U.S.  ENVIRONMENTAL PROTECTION AGENCY (USEPA).  1979.  Water-
      Related Environmental Fate of 129 Priority pollutants
      Washington, D.C.  December 1979.  SPA 440/4-79-029

U.S.  ENVIRONMENTAL PROTECTION AGENCY (USEPA).  1980.  A&bient
      water Quality Criteria for Ethylbenzene.  Office of Water
      Regulations and Standards, Criteria and Standards Division,
      Washington, D.C. ' October 1980.  EPA 440/5-80-048

U.S.  ENVIRONMENTAL PROTECTION AGENCY (USEPA).  1984.  Health
      Effects Assessment^for Ethylbenzene.  Environmental Criteria
      and Assessment Office, Cincinnati, Ohio,   September 1984.
      ECAO-CIN-H008  (Final Draft)

VERSCHUEREN, K.  1977.  Handbook of Environmental Data on Organic
      Chemicals.  Van Nostrand Reinhold Co., Mew York.  €59 pages

WEAST, R.S., ed.  1981.  Handbook of Chemistry and Physics.
      62nd ed.  CRC Press, Cleveland, Ohio.  2332 pages

Ethylbeniene
Page  3
October 1985                                    	
                                                           looatM

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                  ETHYLENE AND DIETHYLENE GLYCOL
 Summary
      Ethylene and diethylene glycol produce similar toxic ef-
 fects.  Both caused bladder stones, severe kidney damage, and
 moderate liver damage in rats when administered chronically
 in the diet.  Inhalation exposure causes nausea, throat irrita-
 tion, and dizziness,  Musculoskeletal abnormalities and crano-
 facial defects were observed in the offspring of pregnant rats
 given high doses of ethylene glycol orally.


 CAS Numbers  Ethylene glycol:  107-21-1
              Diethylene glycol:  111-46*6

 Chemical formula:  Ethylene glycol:  €214(08)2
                    Diethylene glycol:  0(C2H4OH)2

 IUPAC flame;  Sthylene glycols 1,2-Ethanediol
              Diethylene glycol:  2,2-Oxydiethanol

 Important Synonyms and Txade Names:

      Sthylene glycol: Ethylene alcohol, 1, 2-dihydroxy ethane,
                       glycol
      Diethylene glycol:  bis (2-Hydroxyethyl} ether, diglycol,
                          ethylene diglycol


 Chemical and Physical Properties

 Molecular Weight:  Ethylene glycol: €2
                    Diethylene glycol:  106

 Boiling folnti  Ethylene glycol: 1S7»C
                 Diethylene glycol:  24S*C

 Melting Point:  Ethylene flycoli -13.S«C
                 Diethylene flycolt  -10 •€

 Specific Gravity:  1.12 at 20*C

 Solubility in Waters  Soluble in water

 Solubility in Organic*: v Soluble in alcohol, ether, and acetone

 Log Octanol/Water Partition Coefficient:

      Sthylene glycol:  -2 (calculated)
      Dtethylene glycol:  -1.4 (calculated)


 Ethylene and diethyltnt glycol
 *>ge 1
 October 19S5
Preceding page blank

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Vapor  Pressure:  Ethylene  glycol:  0.05 am Hg  at  20*C
                 Diethylene  glycol:   <0.01 aa Hg at 20*C

Vapor  Density:  Ethylene glycols  2.14
                Ditthylenc glycol:   3.66

Flash  Points  Ethylenc  glycol:  116»C
              Diethylene glycol:   124*C


Transport  and fatt

     The limited information on  the  transport and fate of  ethyl-
ene and diethylene glycol  suggests that they  are unlikely  to
volatilize and that biodegradation in soil or surface water
is probably an important fate process for both compounds.
Their  high solubilities and  lot*  log  octanol/water  partition
coefficients suggest that  they move  freely in water.  Oxidation
aay be an  important fate process  In  surface water.


Health Effects

     The lethal oral dose  of ethylene glycol  for human3 is
approximately 1.4 ml/kg, or  100 ml for an adult  man weighing
70 kg.  Children are apparently less susceptible than adults
to ethylene glycol poisoning.  Zngestlon of the  compound can
lead to prostration or  unconsciousness, accoapanied by metabolic
acidosis and renal damage.

     Inhalation exposure to  aore  than 140 mg/m3  of ethylene
glycol causes irritation of  the throat, aild  headache, and
possibly pain in the lower back.  lye irritation from splashing
liquid or exposure to vapor  is possible; in one  study, workers
developed nystagmus when exposed  to  high levels  of ethylene
glycol vapor.  It has not  been established that  ethylene glycol
is a skin irritant, although transient, aild  irritation is
possible.

     In one chronic study, rats that were fed diets containing
It or  2% ethylene glycol (approxiaately SOO to 1,000 ag/kg/day)
for 2 years had shorter life spans,  developed calcium oxalate
bladder stones, and suffered from centrilobular  liver degener-
ation  and severe injury to the renal tubules.  Ethylene glycol
is aetabolixed in the body to oxalic acid, which is deposited
in the kidney as calcium, oxalate.  The syaptoas  of ethylene
glycol poisoning—metabolic  acidosis and renal damage—have
been prevented in monkeys  by the  administration  of alcohol
dehydrogenase inhibitors.

     Ithylene glycol is currently being tested for carcinogen-
icity  by the National Toxicology frograa.  it has  been reported


Ethylene and diethylene glycol
Page 2
October 1985

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that it inhibits DMA synthesis and causes mutations in cultured
mouse 1/iiphocytes.  The reproductive and teratogenic effects of
ethylene glycol have not been determined conclusively, but cran-
iofacial defects and musculoskeletal abnormalities were reported
in rat fetuses when very high doses of ethylene glycol were ad-
ministered orally to pregnant females.

     Ethylene glycol is less toxic to many animal species than
it is to humans,  for example, the oral LD5Q for rats is 4.7 g/Hg;
for mice, 7.5 g/kgj and for guinea pigs, 6.1 g/kg.  The dermal
LD.Q for rabbits is 19.5 g/kg.  Eye irritation has been reported
in rabbits.and rats after exposure to airborne concentrations
of 12 tng/rn  for 3 days.

     Diethylene glycol causes symptoms similar to those produced
by ethylene glycol:  nausea, dizziness, and severe kidney damage,
followed by oligurea or anuria.  The lethal oral dose for humans
is approximately 1 ml/kg.

     In a 2-year study, diethylene glycol fed to rats at dietary
concentrations of 4% (approximately 2,000 ag/kg/day) caused lower
growth rates, bladder stones, severe kidney damage, and moderate
liver damage.  Although there are reports that diethylene glycol
causes bladder tumors in rats, these tumors are thought to
be the result of mechanical irritation caused by calcium oxalate
stones in the bladder.  Diethylene glycol has not been reported
to be mutagenic.  Its reproductive and teratological effects
are not known.

     The oral LD-Q foe the mouse is 23*7 g/kg, and for the
guinea pig it is 7.8 g/kg.  Humans are more than 13 times more
sensitive to diethylene glycol poisoning than rats.  The dermal
LD5Q for rabbits is 11.9 g/kg.


Toxicity to Wildlife and Doaestie Animals

     Only limited information on the toxicity of ethylene glycol
and diethylene glycol to wildlife is available.  Concentrations
of 250 mg/liter of ethylene glycol are toxic to gseudoinonas
putidai Chlorella pyrenoidoaa is killed by 180 mg/litec.The
24-hour LD.Q for goldfish is more than 5,000 mg/liter.  For
diethylene glycol. Inhibition of cell multiplication in ?seudo-
monas putida starts at 8,000 mg/liter.  Toxicity to the alga
MicrQcy8tTi"aeruginosa itatts at 1,700 mg/liter.  The 24-hour
     for goldfish is more than 5,000 mg/liter.  Bioaccunraiation
     not occur.
Ethylene and diethylene glycol
Page 3
October 1985

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Regulations and Standards

ACGIH Threshold Limit Value*

     Ethylene glycol: 125 »g/m3 Ceiling Level


REFERENCES

AMERICAN CONFERENCE OP GOVERNMENTAL INDUSTRIAL IY6IENISTS (ACGIH),
     1980.  Documentation of the Threshold Limit Values.  4th ed.
     Cincinnati, Ohio.  488 pages

LYMAN, W.J., REEHL, W.F., and ROSENBLATT, D.H.  1982.  Handbook
     of Chemical Property Estimation Methods:  Environmental
     Behavior of Organic Compounds,  McGraw-Hill look Co.,
     New York

THE MERCK INDEX.  1976.  9th ed.  Windholz, M., ed.  Merck
     and Co., Rahway, New Jersey

NATIONAL INSTITUTE FOR OCCUPATIONAL SAFETY AND HEALTH (NIOSH).
     1984,  Registry of Toxic Effects of Chemical Substances.
     Data Base.  Washington, D.C.  October 1984

SAX, N.I.  1975.  Dangerous Properties of Industrial Materials.
     4th ed.  van Nostrand Reinhold Co., New York.  1,258 pages

U.S. ENVIRONMENTAL PROTECTION AGENCY (USEPA).  1979.  Water-
     Related Environmental Fate of 129 Priority Pollutants.
     Washington, D.C.  December 1979.  ZPA 440/4-79-029

VERSCHUEREN, K.  1977.  Handbook of Environmental Data on Organic
    * Chemicals.  Van Nostrand Reinhold Co., New York.  €59 pages

WEAST, R.S., ed.  1981.  Handbook of Chemistry and Physics.
     62nd ed.  CRC Press, Cleveland, Ohio.  2,332 pages
Ethylene and diethylene glycol
Page 4
October 1985

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                           ETHYL ETHIR
Summary
     Ethyl ether produced adverse reproductive effects in the
offspring of pregnant rats and alee after the administration of
a single anesthetic dose.  It is a aild akin and eye irritant.
CAS Number:  60-29-7
Chemical Formula:  C-H.OC-H.
IOPAC Name:  Ethoxyethane
Important Synonyms and Trade Names:  Oiethylether, ethoxyethane,
                                     ethyloxide, diethyloxide,
                                     sulfuric ether

Chemical and Physical Properties
Molecular Weight:  74.12
Boiling Points   34.5*C
Melting Point:   -116.2°C
Specific Gravity?  0.7138 at 20"C
Solubility in Water:  60,000 mg/liter at 2S*C
Solubility in Organics:  Soluble in alcohol, acetone, benzene,
                         and chloroform
Log Octanol/Water Partition Coefficient:  1.4 (calculated)
vapor Pressure:  442 aa Eg at 20*C
Vapor Density:   2*56
Flash Points  -45»C

Transport and Fate
     No information on the transport and fate of ethyl ether
was found in the literature reviewed.
     From information on the chemical and physical properties
of ether, it appears that volatilization would be an important

Ethyl ether
Page 1
October 1985
                                                 ^J Qanwtt Ammacmtam
                           Sffel

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transport pathway  from  soil.  Ethyl ether reacts slowly with
air  to lorn explosive peroxides.  High solubility and high
vapor density would limit volatilization somewhat and suggest
that transport in  groundwater nay also occur.  Ethyl ether has
a low log octanol/water partition coefficient and therefore
probably is not sorbed  to any significant extent.


Health Effects

     No information on  the carcinogenicity of ether was reported
in the literature  reviewed.  Ethyl ether inhibited DNA repair
in an assay using  Escherichia coli.  Pregnant female rats and nice
were anesthetized  with ethyl ether for 1 hour either early
or late in gestation  {Schwetz and Becker 1970).  In mice, exposure
to ethyl ether during early embryogenesls caused a significant
increase in resocptions and decrease in the length of fetal
long bones.  Early or late exposure caused an increase in the
incidence of generalized edema, missing sternum, unossified
phalanges, and missing cervical vertebrae.  In rats, anesthesia
during early or late embryogenesis decreased fetal body weight
and the length of  the long bones.

     Ether at high concentrations (greater than 100 g/m ) causes
narcosis and general anesthesia.  It will cause minor skin
and eye irritation at 90 mg/m .  The oral LD-n of ethyl ether
in the rat is 1,215 mg/kg.                  3U


Toxicitv to Wildlife and Domestic Animals

     Ho information on the toxicity of ethyl ether to wildlife
or domestic animals was found in the literature reviewed.


Reg u1a tion and S t and ards

OSHA Standard (air)2  1,200 mg/n3 TWA

ACGIH Threshold Limit Values:  1,200 mf/m* TWA
                               1,500 mg/m4 S.TEL


REFERENCES

AMERICAN CONFERENCE OF GOVERNMENTAL INDUSTRIAL HYGIENISTS (ACGIH).
     19SO.  Documentation of the Threshold Limit Values.  4th ed.
     Cincinnati, Ohio.  t8S pages

AMERICAN INDUSTRIAL HYGIENE ASSOCIATION (AIHA).  1978.  Hygienic
     Guide Series.  Ethyl ether.  AIHA, Akron, Obio
Ethyl ether
Page 2
October 1985

-------
THE MERCK INDEX.  1976.  9th «d.  Windholz, M., ed.  Merck
     and Co., Rahway, New Jersey

NATIONAL INSTITUTE FOR OCCUPATIONAL SAFETY AND 1EALT1 (NIOSHJ.
     If84.  Registry of Toxic Effects of Chemical Substances.
     Data Base.  Washington, D.C.  July 1914

SAX, N.I.  1975.  Dangerous Properties of Industrial Materials.
     4th ed.  Van Nostrand Reinhold Co., New York.  1,258 pages

SCHWETZ, B.A., and BECKER, B.A.  1970.  Embryotoxicity and
     fetal malformations of rats and mice due to maternally
     administered ether.  Tozicol. Appl. Pharmacol. 17:275

U.S. ENVIRONMENTAL PROTECTION AGENCY (DSEPA).  1979.  Hater-
     Related Environmental 7ate of 129 Priority Pollutants.
     Washington, D.C.  December 1979.  1PA 440/4-79-029

VERSCHUEKEN, X.  1977.  Handbook of Environmental Data on Organic
     Chemicals.  Van Nostrand Reinhold Co., New York.  659 pages

WEAST,  R.E., ed.  1981.  Handbook of Chemistry and Physics.
     62nd ed.  CRC Press, Cleveland, Ohio.  2,332 pages
Ethyl ethtc                                           •
Page 3                                            Coement
October 1985                                      w

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                         ETHYL HEXANEDIOL
Summary
     Ethyl hexanediol  is quite  irritating to  the eyes.

CAS Number:   94-96-2
Chemical Formulas  CaH,-(OIK
                    8  Xp    2
IUPAC Hame:   2-Bthyl-l,3-hexanediol
Important Synonyms and  Trade Namesi   Carbide 6-12, Cmpd 6-12
                                      insect  repellent, ethohexadiol
                                      ethyl hexy lene glycol,
                                      2-ethyl-3-propyl-1,3~
                                      propanediol, Rutgers €12
Chemical and  Physical Properties
Molecular Weight:  146.26
Boiling Point:  243.PC
Specific Gravitys  0.9422 at 20°C
Solubility in Water:  6000 ag/liter
Solubility in Organics:  Soluble in alcohol, ehter, propylene
                         glycol, and castor oil
Log Octanol/Water Partition Coefficient:  1 (calculated)
Vapor Pressure:  <0.01  BUB Hg at 20*C
Vapor Density}  5.03
Plash Point:  127*C (open cup)

Transport and Pate
     Mo information on  the transport and fate of ethyl hexanedi-
ol was available in the sources reviewed.  Ethyl hexanediol is
fairly soluble in water, has a low vapor pressure, and therefore
probably is not volatile.  Reactions typical of alcohols, such
as oxidation or esterification, are likely to be important in
determining the fate of ethyl hexanediol.
Ethyl hexanediol
Page 1
October 1985
  Preceding page blank

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Health Effects

     Only limited information was available on ethyl hcxanediol
in the sources reviewed.  The compound is quit* irritating
to the *y« but does not irritate the skin.  The oral LD50 in
the rat it 1,400 mgAg, and the dermal LDcn for toe rabolt
is 2,000 »g/kg.                          5g


Toxicity to Wildlife and Domestic Animals

     No information on the toxicity of ethyl hexanediol to
wildlife was found in the literature reviewed.  Jin oral LO.Q
of 1,400 ag/kg was detexained foe the chicken.


REFERENCES

LYMAN, H.J., REEHL, W.F., and ROSENBLATT, D.H.  1982.  Handbook
     of Chemical Property Estimation Methods:  Environmental
     Behavior of Organic Compounds.  McGraw-Hill Book Co.,
     New York

THE MERCK INDEX.  1976.  9th ed.  Windholx, N.f ed.  Merck
     and Co., Eahway, New Jersey

NATIONAL INSTITUTE FOR OCCUPATIONAL SAFETY AND HEALTH (NIOSH).
     1984.  Registry of Toxic Effects of Chemical Substances.
     Data Base.  Washington, D.C.  October 1984

SAX, N.I.  1975.  Dangerous Properties of Industrial Materials.
     4th ed.  Van Nostrand Reinhold Co., New York.  1,258 pages

WE AST, R.E., ed.  1981.  Handbook of Cheaistry and Physics.
    ' 62nd ed.  CRC Press, Cleveland, Ohio.  2,332 pages
Bthyl hexanediol
»age 2
October 1985

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                    BIS C 2-ETHYLR1XYL)PHTHALATB
Surnma r y
     bis{2-Ethylhexyl)phthalate  (DEEP) la probably persistent
in the environment.  It is carcinogenic in rats and mice, causing
hepatocellular carcinomas.  Teratogenic and reproductive effects
have been observed in experimental animals.  Chronic exposure
to DEHP retarded growth and increased liver and kidney weights
in animals.
CAS Number:  117-81-7
Chemical Formula?  C
IUPAC Name;  bis(2-Ethylhexyl)ester phthalic acid
Important Synonyms and Trade Names:  DlfEP, Di(2-ethylhexyl)phthalat
                                     bis(2-ethylhexyl)ester
                                     phthalic acid
Chemical and Physical Properties
Molecular Weightj  391.0
Boiling Point:   383.9*C at 5 mm Hg
Melting Point:   -SO'C
Specific Gravity:  1.9i5
Solubility In Water;  0.4 ag/liter at 25*C
Solubility in Organic*;  Miseible with mineral oil and hexane
Log Octanol/Water Partition Coefficients  5.3
Vapor Pressures  2 x 10*  an Hg at 20*C
Flash Pointi  21S.33«C
                         *n
Transport and Fate
     bis(2-EthylhexylJphthalate (DEHP) is the most thoroughly
studied of the phthalate esters.  It probably hydrolyzes in
surface waters, but at such a slow rate  that this process is
not environmentally significant under most conditions.  Photo-

bis(2-2thylhexyl)phthalate
Page 1
October liBS

-------
lysis and oxidation do not appear to be Important environmental
fate processes.  Although some researchers suggest that volati-
lization of DEHP from aqueous solution may be significant under
some conditions, it probably is not an important environmental
transport process in natural waters.  In contrast, there is
evidence that this compound can be slowly volatilized from
DEHP-eontaining materials at relatively high temperatures.
Consequently, some atmospheric dispersion of DEHP due to vapori-
zation during manufacturer use, or waste disposal probably
occurs.
   .*         *
   .-"Adsorption onto suspended solids and particulate natter
and complexation with natural organic substances are probably
the- most important environmental transport processes for DEHP.
The log oetanol/water partition coefficient for DEHP suggests
that this compound would be adsorbed onto particulars high
in organic matter.  This contention is supported by the fact
that phthalate esters are commonly found in freshwater and
saltwater sediment samples.  DEHP can be dispersed from sources
of manufacture and use to aquatic and terrestrial systems by
eomplexation with natural organic substances.  It readily inter-
acts with the fulvie acid present in humie substances in water
and soil i forming a complex that is very soluble in water.

     A variety of unicellular and multicellular organisms take
up and accumulate DEHP, and bioaccunulation is considered an
important fate process.  Biodegradation is also considered
an important fate process in aquatic systems and soil.  DEHP
is degraded under most conditions and can be metabolized by
multicellular organisms.  Therefore, it is unlikely that long-
term biomagnif ication occurs.

     Analysis using EPA's Exposure Analysis Modeling System
suggests that chemical and biochemical transformation processes
for DEHP are slow and that transport processes will predominate
both in ecosystems that have long retention tines (ponds, lakes)
and in those that have short retention times (rivers) .  If
the input of DEHP remains constant, its concentration is expected
to increase in aquatic ecosystems*  If the input stops, the
DEHP present is expected to persist for an undetermined length
of time.  The ocean* are the ultimate sink for DEHP introduced
into unimpeded rivers.


Health Effects

     DEHP is reported to be carcinogenic in rats and mice,
causing increased incidences of hepatocellular carcinomas or
neoplastic nodules after oral administration CRT? 1982).  Its
status as a human carcinogen is considered indeterminate by
the International Agency for Research on Cancer (I ARC).  The
results of dominant lethal experiments with mice suggest that


bis (2-Ethylhexyl) phthalate
fage 2
October 1985
                                                                    "J

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DEHP is mutagenie when injected intraperitoneally.  However,
most experiments conducted with microorganisms and mammalian
cells have failed to demonstrate genoto*ie activity.  Teratogenic
and ietotoxic effects have been observed in experimental animals
after oral and intraperitoneal administration.  Other reproduc-
tive effects, including testicular changes in rats and mice,
have also been reported.

     DEHP appears to have a relatively low toxicity in experi-
mental animals.  The oral, intrapetitoneal, and intravenous
1D50 values reported for DEHP in rats are 31 g/kg, 30.7 g/kg,
ana 0.25 g/kg, respectively.  DEHP is poorly absorbed through
the skin, and no irritant response or sensitizing potential
from dermal application has been noted in experimental animals
or humans.

     Chronic exposure to relatively high concentrations of DEHP
in the diet has caused retardation of growth and increased
liver and kidney weights in experimental animals.


Toxicity to wildlife and Domestic Animals

     Acute median effect values ranged from 1,000 to 11,100
         DEHP for the freshwater cladoceran Daphnia magna.
The LC.n values for the midge, scud, and bluegill all exceeded
the hifnest concentrations tested, which were 18,000, 32,000,
and 770,000 pg/liter, respectively.  As these values are greater
than the water solubility of the chemical, it is unlikely that
DEHP will be acutely toxic to organisms in natural waters.  In
a chronic toxicity test with Daphnia magna, significant repro~
ductive impairment was found at the lowest concentration tested,
3 pg/3iter.  A chronic toxicity value of S.4 M9/liter was reported
for the rainbow trout.  No acute or chronic values were reported
for saltwater invertebrates or vertebrates.  Reported bioconcen-
tration factors for DEHP in fish and invertebrates range from
14 to 2,680.

     Although insufficient data were presented to calculate
the acute-chronic ratio for DEHP, it is apparently on the order
of 100 to 1,000.  Therefore, acute exposure to the chemical
is unlikely to affect aquatic organisms adversely, but chronic
exposure may^ have detrimental effects on the environment.
           , ' T

Regulations and Standards

Ambient Water Quality Criteria (OSEPA)s

     Aquatic Life

     The available data are not adequate for establishing criteria


bis(2-sthylhexyl)phthalit«
Page 3
October 1965

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     £or bisu-ethylhexyljphtnaiate or for phthalate esters
     as a group,

     Human Health

     Criterion:  15 nig/liter

ACGIH Threshold Limit Values:  5 ng/m3.TWA
                               10 mg/ar STEL
REFERENCES

AMERICAN CONFERENCE OF GOVERNMENTAL INDUSTRIAL HYGISNISTS  (ACGIH)
     1910.  Documentation of the Threshold Limit Values.   4th
     ed.  Cincinnati, Ohio.  48S pages

NATIONAL INSTITUTE FOR OCCUPATIONAL SAFETY AND HEALTH  (NIOSH).
     1983..  Registry of Toxic Effects of Chemical Substances.
     Data Base.  Washington, D.C.  October 1983

NATIONAL TOXICOLOGY PROGRAM  (NTP).  1582.  National Toxicology
     Program  (NT?) Technical Report on the Carcinogenesis Bio-
     assay of Di{2-£thylhexyl)Phthalate  (CAS No. 117-81-7) in
     F344 Rats and B6C3F, Mice  (Feed Study), Bethesda, Maryland.
     March 1982.  NTP-80-37.  NIH Publication No. 82-1773

NATIONAL TOXICOLOGY PROGRAM AND THE INTERAGENCY REGULATORY
     LIAISON GROUP.  1982.  The Conference on Phthalates.
     Environ. Health Perspect. 45:1-153

SAX, N.I.  1975.  Dangerous Properties of Industrial Materials.
     4th ed.  Van Nostrand Reinhold Co., New York.  1,258 pages

U.S. ENVIRONMENTAL PROTECTION AGENCY (USEPA).  1979.  Water-
     Related Environmental Fate of 129 Priority Pollutants.
     Washington, D.C.  December 1979.  EPA 440/4-79-029

U.S. ENVIRONMENTAL PROTECTION AGENCY (USEPA).  1980.  Ambient
     Water Quality Criteria for Phthalate Esters.  Office of
     Water Regulations and Standards, Criteria and Standards
     Division, Washington, D.C.  October 1980.  EPA 440/5-80-067

WEAST, R.E., ed.  1981.  Handbook of Chemistry and Physics.
     62nd ed.  CRC Press, Cleveland, Ohio.  2332 pages
bis(2-Ethylhexyl)phthalate
Page 4
October 1985
                                                                 J

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                           PLUORANTHENE
Summary
    . Fluoranthene  is  a polycyclic aromatic hydrocarbon  (PAH)
 It  is  probably persistent  in  the environment.  Fluoranthene
 doa not appear to  be  a complete carcinogen, but it has been
 shown  to be a potent  cocareinogen in animal test systems.
CAS Number:  206-44-0

Chemical Formula*  cigaio


Chemical and Physical Properties

Molecular Weight;  202.26

Boiling Point:  Approximately 375*C

Melting Points  111«C

Specific Gravity;  1.252 at 0*C

Solubility in Waters  0.26 mg/liter

Solubility in Organicsi  Soluble in ethanol, ether, benzene,
                         chloroform, acetic acid, and carbon
                         diaulfide

Log Octanol/Water Partition Coefficients  5.33  (calculated)

vapor Pressures 10*  to 10*"* ma Hg at 20*C  (estimated)


Transport and Fate

     Much of the information concerning transport and fate is
inferred from data for polycyclic aromatic hydrocarbons  (?AHs)
in general because of a lack of specific information on  fluor-
anthene.  Rapid, direct photolysis of fluoranthene to quinones
may occur in aqueous solution.  The oxidation of fluoranthene
is probably too slow to be a significant environmental process,
and the available data suggest that volatilisation generally
is not an important transport process for fluoranthene.  The
calculated log octanol/water partition coefficient of 5.33
indicates that the compound should be strongly adsorbed  onto
particulate natter, especially participates high in organic
content.  It is likely that fluoranthene can be transported

Fluoranthene
Page 1
October 1985

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 as  adsorbed  natter  on  suspended  particulates  in  alt  or  water.
 Data  for  PAHa  in  general  indicate  that  fluoranthene  will  accu-
 mulate  in the  sediment and  biota of  the aquatic  environment
 and that  adsorption is probably  the  dominant  aquatic transport
 process.

      Data for  a variety of  PAHs  suggest that  bioaccumulation
 is  a  short-term process,  and  long-term  partitioning  into  biota
 is  not  a  significant fate process,   fluoranthene can be metab-
 olized  by nulticellular organisms  and degraded by microbes.
 Degradation  by mammals is likely to  be  incomplete? the parent
 compound  and the  metabolites  are excreted by  the urinary  system.
 Biodegradatlon by microorganisms is  probably  the ultimate fate
 process.   Biodegradation  generally appears  to be slower in
 aquatic systems than in soil.  However,  it  may be important
 in  those  aquatic  systems  that are  chronically affected by PAH
 contamination.  Fluoranthene  is  stable  enough in air to be
 transported  over  relatively large  distances.


 Health  Effects

      There is  no  information  concerning the carcinogenicity
 of  fluoranthene in  humans,  and fluoranthene shows no activity
 as  a  complete  carcinogen  in experimental animals.  However,
 fluoranthene appears to possess  potent  cocarcinogenic activity
 in  test animals.  Fluoranthene has displayed  no  atutagenlc acti-
 vity  in in vitro  bacterial  teat  systems.  NO  other information
 Is  available concerning its potential mutagenic  or teratogenic
 effects,  nor with regard  to its  acute or chronic toxlcity to
 humans.   Results  from  animal  studies indicate that fluoranthene
 has relatively low  acute  toxicity.   Where deaths of  experimental
 animals have occurred,  no information concerning target organs
 or  specific  causes  of  death has  been reported.   Descriptions
 of  chronic toxici-ty are limited  to reports  of mortality produced
 in mice by repeated dermal  application  or subcutaneous injection.


 Toxicity  to  wildlife and  Domestic  Animals

     Among freshwater  species, the bluegill,  with a  96-hour
 liC-Q  value of  3,ISO ug/liter, 1* mote sensitive  to fluoranthene
 thin  the  cladoceran Daphnia macna, with a 48-hour BCSO value
 of 325*000 ^g/liter.   No  chronic data are available  for fresh-
 water organisms.  Among saltwater  species,  toe 96-hour LC.Q
 values  for the mysid shrimp and  a  polychaete  are 40  and 500 Mg/liter,
 respectively.  The  96-hour  LC-B  value for the sheepshead  minnow
 is greater than 560,000 jig/litir.  The  chronic value and  acute-
 chronic ratio  for the  mysid shrimp are  16 tig/liter and 2.5,
 respectively.  The  freshwater and  saltwater algal species tested
 exhibit similar sensitivities to fluoranthene, with  EC.Q  values
 of about  50,000 ug/littr.   There if  evidence  of  fluoranehene


Fluoranthene
 Page 2
October 1985

-------
accumulation in edible aquatic organisms, although no measured,
steady-state bioconcentration factors art available for fresh-
water or saltwater organisms.


Regulations and Standards

Ambient Water Quality Criteria (USEPA}s

     Aquatic Life

     The available data are not adequate for establishing criteria,
     However, EPA did report the lowest concentrations of fluor-
     anthene known to cause toxic effects in aquatic organisms.

     Freshwater

          Acute toxicity:  3,980 ug/liter
          Chronic toxicity:  No available data

     Saltwater

          Acute toxicity!  40 ng/liter
          Chronic toxicity:  16 ug/liter

     Human Health

     Criterion:  42 ug/liter


REFERENCES

NATIONAL INSTITUTE FOR OCCUPATIONAL SAFETY AND HEALTH (NIOSH).
     1983.  Registry of Toxic Effects of Chemical Substances,
     Data Base.  Washington, D.C.  October 1983

U.S. ENVIRONMENTAL PROTECTION AGENCY  (USEPA).  1979.  Water-
     Related Environmental Fate of 129 Priority Pollutants.
     Washington, D.C.  December 1979.  EPA 440/4-79-029

U.S. ENVIRONMENTAL PROTECTION AGENCY  (USEPA).  1980.  Ambient
     Watte Quality Criteria for Pluorant'hene.  Office of Water
     Regulations and Standards, Criteria and Standards Division,
     Washington, D.C. ' October 1980.  EPA 440/5-80-049

WEAST. R.E., ed.  1981.v Handbook of Chemistry and Physics.
     62nd ed.  CRC Press, Cleveland, Ohio.  2332 pages
Fluoranthen*
Page 3
October 198 S                                    flosnwnt AMOCMCM

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                           FORMALDEHYDE
Summary
     Formaldehyde has been shown to produce nasal tumors in
rats, and there is suggestive evidence that it produces the
sane type of tumor in humans.  Inhalation exposure to formal-
dehyde causes respiratory Irritation and can also produce local-
ized effects in the nose, throat, and lungs.  In addition,
formaldehyde can irritate the skin and cause allergic dermatitis
in susceptible individuals.


CAS Number;  50-00-0

Chemical Formula;  CH-O

IUPAC Name:  Methanal

Important Synonyms and Trade Names:  Methanal, Formalin
                                     (formaldehyde solution)


Chemical and. Physical Properties

Molecular Weight:  30.03

Boiling Point:  19.5*C

Melting Points  -92»C

Specific Gravity:  0.867 at 20*C

Solubility in Water:  Undergoes solvation in water or methinol

Solubility in Organics:  Soluble in chloroform, ether, and
                         toluene

Vapor Pressure:  760 mm Ig at 19.S*C

Vapor Densitys  1.075

Flash Point:  300*C

                        s.
Transport and Fate

     Formaldehyde is a gas at ambient temperatures so the air
will be a major route of transport.  In water, formaldehyde
is rapidly hydrated and converted to aethylene glycol and poly-
oxynethylene glycols, however, it can volatilize as formaldehyde.


Formaldehyde
fage 1
October 1985
    Preceding page blank

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Formaldehyde  readily  adsorb*  to clay soils but  sorption  to
•oil  with  smaller  amounts of  organic material is probably neg-
ligible.

      Photolysis of formaldehyde occurs  in the lower  troposphere
by  two primary processes.  One process  predominates  at wave-
lengths of  290 to  313 na and  the other  predominates  at wave-
lengths of  313 to  360 na.  Reported products of formaldehyde
photolysis  are formyl radicals and water.  The  estimated half-
life  of formaldehyde  in sunlight is about 75 ainutes.  In water,
formaldehyde  is hydrated to aethylene glycol and polyoxymethylene
glycols which do not  undergo  photolysis.  Further degradation
occurs in water, primarily due to biodegradation.


Health Effects

      Formaldehyde  has been shown to produce nasal tumors in
rats, and there is suggestive evidence  that it  produces  the
same  type of  tuaor in humans  (Siegel et al. 1983).   it has
been  shown  that formaldehyde  is a 'weak* autagen producing
gene  mutations and chromosomal abberrations in  a variety of
laboratory  test systems.  Formaldehyde  has also caused cell
transformation in  cell culture systems.  Formaldehyde has not
been  shown  to be teratogenic  or to cause reproductive toxicity
in  animal studies.  However,  the studies have not been adequate
to  fully assess these toxicities.

      Formaldehyde  is  a respiratory irritant and has  been found
to  produce  localized effects  in the nose, throat, and tracheo-
bronchial tree of  exposed individuals.  Irritation of the skin
has also been reported.  In addition, an allergic dermatitis
has been produced  in  some people exposed to formaldehyde.  The
inhalation  LD50 *n rats **9 reported to be 100 ag/m  .


Toxicitv to Wildlife  and Domestic Animals

      Data concerning  toxicity to wildlife and domestic animals
are not available.
Regulations and Standards

NIOSH Recommended Standard:  0.$ mg/m

OSHA Standard  (Air)i  3.6 mg/m3 TWA

ACGIH Threshold Limit Value:   1.5  (Suspect Carcinogen)
Formaldehyde
Page 2
October 19S5

-------
REFERENCES

AMERICAN CONFERENCE OF GOVERNMENTAL INDUSTRIAL HYGIENISTS (ACGIH)
     1980.  Documentation of the Threshold Limit Values.  4th ed.
     Cincinnati, Ohio.  488 pages

FASSETT, D.W.  1963. Aldehydes and acetals.  In fatty, F.A.,
     ed.  Industrial Hygiene and Toxicology.  2nd ed.  Inter-
     science Publishers, New York

THE MERCK INDEX.  1976.  9th «d.  Windholz, M., ed.  Merck
     and Co., Rahway, Mew Jersey

NATIONAL INSTITUTE FOR OCCUPATIONAL SAFETY AND HEALTH (NIOSH).
     1977.  Criteria for a Recommended Standard—Occupational
     Exposure to Formaldehyde.  Washington, D.C.  DHEW Publi-
     cation No. (NIOSH) 77-126

SELIXQFP, I.J., and HAMMOND, E.G.  1981.  Carcinogenicity of
     Formaldehyde.  Final Report.  Environmental sciences Labor-
     atory, Mount Sinai School of Medicine, City University
     of New York

SIEGEL, D.M., FRANCOS* V.H., and SCHNEIDE1MAH, M.A.  1983.
     Formaldehyde risk assessement for occupationally exposed
     workers.  Regulatory Toxicol. Pharmacol. 3:355-371

U.S. ENVIRONMENTAL PROTECTION AGENCY (DSEPA).  1981.  Technical
     Document:  Formaldehyde.  Office of Pesticides and Toxic
     Substances* Washington, D.C.  November 16* 1981
Formaldehyde
Page 3
October 1985
                            303

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                            HEPTACHLOR
 Summary;
      Heptachlor  Is  an  organochlortne  pesticide.  Together  with
 its  active metabolite,  heptachlor  epoxide,  it  is very persistent
 in  the  environment.  When  administered  orally  to nice, both
 substances cause liver  tumors.  They  also have mutagenic effects,
 These chemicals  have a  number of reproductive  and  teratogenic
 effects,  including  decreased litter size, shortened  life span
 of  suckling  young,  and  the development  of cataracts  in offspring,
 The  acute toxiclty  of  both heptachlor and heptachlor epoxide
 is very high.  Chronic  exposure induces liver  changes and  nay
 cause kidney damaqe.  Heptachlor is also highly toxic to fish
 and  wildlife.
 BackgroundInformation

     Technical heptachlor  is  a  complex mixture containing  approxi-
 mately  721  heptachlor and  28% related compounds.   It  is  a  soft
 wax  with  a  melting point of 46-74*C.

 CAS.  Numbers   76-44-8

 Chemical  Formula:  C,QH.C17

 IUPAC Name:   1,4,S»6,7,8,8-leptachloro-3a,4f7,7a-tetrahydro-
              4,7-methanoindene


 Chemical  and  Physical Properties

 Molecular Weights  373.3

 Melting Point:   95-96»C

 Specific  Gravityt  1*97-1.59  at 9mC

 solubility  in Water:  0.056 to  0.180 mg/liter at  25-29°C
                      depending on particle  size

 Solubility  in Ocganicst  Soluble  in ethanol, ether, benzene,
                         acetone, carbon  tetrachloride,  xylene,
                         kerosene, cyclohexanone,  and ligroin

 Vapor Pressures   0.0003 an Eg at  25*C
Heptachlor
page  1
October  1985
Preceding page Wank

-------
 Transport  and Fate

      Heptachlor  and  its  active  aetabolite,  heptaehlor  epoxide,
 are  very persistent  In the  environment,  resisting  chemical
 and  biological breakdown into haralesi  substances.  Sorption
 of heptachlor to sediments  appears  to be an important  process
 for  removal  of the pesticide fron'water, as residue concentra-
 tions in sediment are often much higher  than in water.  Some
 volatilization may also  occur.

      .Heptachlor  and  heptachlor  eposide  bind tightly to soil
 particles  and will persist  for  years in  soil after surface
 application.   However, heptachlor applied as an emulsifiable
 concentrate  is more  readily volatizcd than  when applied as
 a granular formulation.   Certain crops  accumulate  residues
 of these compounds by absorption from the soil.

      Atmospheric transport  of vapors and contaminated  dust
 particles  from soil  application sites can occur.  Heptachlor
 and  heptachlor epoxide are  widespread in ambient air,  but gen-
 erally occur  at  low  concentrations.  However, levels vary both
 geographically and seasonally.


 Health Effects

      Heptachlor  and  heptachlor  epoxide  are  liver carcinogens
 when  administered orally to aiee.   Results  from mutagenicity
 bioassays  suggest that these compounds  also may have genotoxic
 activity.  Reproductive  and teratogenic  effects in rats include
 decreased  litter size, shortened life span  of suckling rats,
 and development  of cataracts in offspring.

      Tests with  laboratory  animals, primarily rodents, demon-
 strate acute  and chronic toxic  effects due  to heptachlor expo-
 sure.  Although  heptachlor  and  heptachlor epoxide are  absorbed
 most  readily  through the gastrointestinal tract, inhalation
 and skin contact are also potential routes  of exposure.  Acute
 exposure by various  routes  can  cause development of hepatic
 vein  thrombi  and can affect the central  nervous system and cause
 death.  Chronic  exposure induces liver changes, affects hepatic
 microsomal enzyme activity, and causes  increased mortality in
 offspring.  The  oral l.0.fl in the rat is  40  «fAf for heptachlor
 and 47 mg/kg  for heptacnior epoxide.

     Although there  are  reports of  acute and chronic toxicity
 in huaana, with  symptoms including  tremors, convulsions, kidney
 damage, respiratory  collapse, and death, details of such episodes
 are not well  documented.  Heptachlor epoxide has been  found
 in a  high percentage of  human adipose tissue samples,  and also
 in human milk samples and biomagnification  of haptachlor/hepta-
 chlor  epoxide occurs.  This compound also has been found in


Heptachlor
Page 2
October 1985
                                                                    -  If
                                                                    • J

-------
the tissues of stillborn infants, suggesting an ability to
cross the placenta and bioaccumulate in the fetus.


Toxicity to Wildlife and Domestic Animals

     Heptachlor is toxic at low concentrations in some aquatic
invertebrate and fish species.  Heptachlor epoxida appears
to be a minor product of heptachlor transformations in aquatic
systems but the capability of different organisms to effect
epoxidation varies.  Mean acute values for freshwater species
range from 0.9 to 78 ng/liter for invertebrates and from 13.1
to 320 pg/liter for fish.  A life cycle test conducted with
the fathead minnow provides a chronic value of 1.26 ug/liter
and an acute-chronic ratio of SO for this species.  Saltwater
mean acute values range from 0.04 to 194 ug/liter for a variety
of fish and invertebrate species.  A chronic value of 1.58 ug/littr
and an acute-chronic ratio of 3.9 are reported for the sheepshead
mi nnow.

     Heptachlor shows a strong tendency to bioaccumule.  it can
concentrate at levels thousands of tines greater than those in
the surrounding water in a variety of aquatic organisms.  Because
of this tendency for bioaccumulation, chronic exposure to levels
greater than 0.004 ug/litei is considered potentially harmful to
aquatic life.  However, this value aay be too high because the
average concentration in a high lipid species will be at FDA ac-
tion levels for human consumption.

     Heptachlor and heptachlor epoxide residues have been found
in a wide variety of wildlife and domestic animal species,
but usually at relatively low levels.  The use of heptachlor
as a seed dressing for cereal grains has been linked to mortality
among granivorous birds and to increased residues in the tissues
of granivorous birds and mammals.  Residues have also been
found in raptors but a causal relationship with observed toxic
effects has not been established.  Increased mortality among
birds, mammals, fish, and aquatic species has been reported in
areas treated with heptachlor.  Heptachlor oe heptachlor epoxide
residues have regularly been found in food and feed crops, meat,
fish, poultry, dairy products, and eggs.  Oral LC5Q values for
heptachlor ranging from 92 to 480 ppm in their disc {around
20 mg/kg body weight) art reported for wild bird species.
Heptachlor
Page 3
October 1985
                         3*1-

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Regulations and Standards
Ambient Watte Quality Criteria  (USEPA):
     Aquatic Life
     Freshwater
          Acute toxicity:  0.52 ug/liter
          Chronic toxicityi  0.0033 |ig/liter
     Saltwater
          Acute toxicity:  0.053 ug/liter
          Chronic toxicity:  0.0036 Mi/liter
     Hunan Health
     Estimates of the carcinogenic risks associated with life-
     tine exposure to various concentrations of heptachlor
     in water are:
     Risk                        Concentration
     10"!                        2.78 ng/liter
     10"!                        0.28 ng/liter
     10"'                        0.028 ng/liter
GAG Unit Risk (USEPA)t  3.37 tag/kg/dayj"1
OSHA standard (skin):  0.5 mg/m3 TWA
ACGIH Threshold Limit Values (akin):  O.S mg/m3 TWA
                                      2 mg/m  STEL

RSF1RENC2S
ATALLAH, ?.H.» WHITACRE, D.M, and 100, B.L.  1979.  Comparative
     volatility of liquid and granular formulations of chlordane
     and heptachlor froa toil.  Bull. Environ. Contaa. Toxicol.
     22t570-574
THE MERCK INDEX.  1976.  9th ed.  Wlndholz, N.r «i.  Merck
     and Co., Rahway, Hew Jersey
SATIONAI, OMICBR IHSTITOfE CRC1).  1977.  Bioaasay of leptachlor
     for Possible Carcinogenicity.  (CAS No. 76-44-8)  NCI
     Careinogenesia Technical Report Series Ho. 9.  Washington,
     D.C.  DHEW Publication No. (NIB} 77-809
Heptachlor
Page 4
October 1985
                               30?

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"N
 >
NATIONAL INSTITUTE FOR OCCUPATIONAL SAFETY AND HEALTH (NIOSH).
     1983.  Registry of Toxic Effects of Chemical Substances.
     Data Base.  Washington, D.C.  October 1983

O.S. ENVIRONMENTAL PROTECTION AGENCY (USEPA).  1971.  Draft
     Environmental Impact Statement Concerning Notice of Intent
     to Cancel Registered Uses of Products Containing Chlordane
     and Heptachlor.  Washington, D.C.  August 1976.
     EPA 540/4-76-003

O.S. ENVIROMENTAL PROTECTION AGENCY (USEPA).  1976.  Pesticidal
     Aspects of Chlordane and Heptachlor in Relation to Man
     and the Environment—A Further Review, 1972-1975.  Washington,
     D.C.  August 1976.  EPA 540/4-76-005

U.S. ENVIRONMENTAL PROTECTION AGENCY (OSEPA).  1979.  Water-
     Related Environmental Fate of 129 Priority Pollutants.
     Washington, D.C.  December 1979.  EPA 440/4-79-029

U.S. ENVIRONMENTAL PROTECTION AGENCY {OSEPA}.  1980.  Ambient
     Water Quality Criteria for Heptachlor.  Office of Water
     Regulations and Standards, Criteria and Standards Division,
     Washington, D.C. 'October 1980.  EPA 440/5-80-052

U.S. ENVIRONMENTAL PROTECTION AGENCY (USEPA).  1985.  Health
     Assessment Document for Dichloronethane (Methylene Chloride).
     Office of Health and Environmental Assessment.  Washington,
     D.C.  February 1985.  EPA 600/8-82/004F

WEAST, R.E., ed.  1981.  Handbook of Chemistry and Physics.
     62nd ed.  CRC Press, Cleveland, Ohio.  2,332 pages

WORTHING, C.R., ed.  1979.  The Pesticide Manuals  A World
     Compendium.  British Crop Protection Council, Croydon,
     England.  655 pages
Heptachlor
Page 5
October 1985

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                         HEXACHLOROBENZENE
 Summary
       Hexachlorobenzene  Is very persistent in the environment
 and can be  bioaccumulated.  It is carcinogenic in nice, rats,
 and hamsters,  causing liver tumors  in all three species and
 tumors of the  spleen and thyroid in hamsters*  There is equivocal
 evidence that  hexachlorobenzene is  teratogenici reproductive
 effects have been  observed in rats  and monkeys.  Humans accidentall
 exposed to  hexachlorobenzene displayed numerous adverse effects,
 including enlarged livers« rheumatoid arthritis-like symptoms,
 and severe  skin  damage.
 CAS Humberi   118-74-1
 Chemical Formula:  c$cl$
 IUPAC Name:   Hexachlorobenzene
 Important  Synonyms and Trade names!  HCB, perchlorobenzene

 Chemical and  Physical Properties
 Molecular Weightt  285
 Boiling Points  32S*C
 Melting Foint:  230«C
 Specific Gravity*  1.57 at 20*C
 Solubility in water*  10 ug/liter at 2S*C
 Solubility in Organic*t  Soluble in acetone, ether, benzene,
                          and chloroform
 Log Octanol/Water partition Coefficients  6.18
 Vapor Pressuret  1 x 10   mm Eg at 20*C
 Vapor Density:  918
 Flash Points  242*C
 Rexachlorobenzene
 Page  1
 October  1985
Preceding page blank

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 Transport and Fate

     Hexachlorobenzene  (RGB)  la persistent  in the  environment.
 Although it has a low vapor pressure,  it may volatilize because
 of  its  low water solubility and high level  of activity in water.
 HCB has * high log octanol/water partition  coefficient and
 therefore would not be  expected to move readily through soil.
 Also, its high specific gravity suggests that it would probably
 move through soil as a  nonaqueous-phase liquid  (NAPL) and not
 necessarily in the, groundwater.

   •** The major fate of  hexachlorobenrene is probably nonpernanent
 sorption to organic material  in the soil and sediment.  Although
 this binding will Immobilize  HCB, it will not do so permanently,
 and desorption may produce continuous/ low-level concentrations
 of  HCB  in the surrounding media*  Organisms can bioaccumulate
 HCB, but it is unclear  whether biomagnification occurs in the
 food chain.  Degradation in the environment, occurs very slowly,
 if  at all.  The two possible  routes of degradation are photolysis,
 possibly assisted by the presence of photosensitizing organic
 materials in aqueous media, and biodegradation by  soil and
 aquatic organisas.


 Health  Effects

     Hexachlorobenzene  is carcinogenic in mice, rats, and hamsters.
 Liver tumors are induced in all three  species.  In addition,
 tumors  of the spleen and thyroid were  induced in HCB-treated
 hamsters (Cabral et al* 1977).  There  is equivocal evidence
 suggesting that HCB is  teratogenic at high  dose levels in rats
 (Khera  1974) and nice (Courtney et al. 197$).  The addition
 of  RGB  to the diets of  rats at 160 ppn (approximately 10 rag/kg/day)
 or  more adversely affects reproduction (Grant et al. 1977).
 HCB has also had adverse effects on reproduction in monkeys
 (latropoulos et al. 1976).  In an epidemic  of HCB  poisoning
 in  Turkey in which the  overall mortality rate among exposed
 persons was about 10%,  951 of the breast-fed infants whose
 mothers were exposed to HCB died.  This incident was caused
 by  consumption of seed  grain  that had been  treated with a fungi-
 cide containing HCB; more than 3,000 people were affected by
 porphyria cutanea tarda, a defect in porphyrln metabolism caused
 by  HCB.  The affected individuals displayed severe skin manifesta-
 tions including photosensitivity, increased pigmentation, bullae
 formation, deep scarring, a permanent increase in  body hair,
 and atrophy of the skin. ' Many children were affected with
 rheumatoid arthritis-like symptoms, and about one-third of
 all victias had enlarged livers (Courtney 1979).   A similar
 effect  on porphyrin metabolism has been seen in experimental
 aniaals fed HCB.  HCB also appears to have  an adverse effect
on  the  immune system in nice, and it is an  inducer of mixed
 function oxidase enzymes in the liver.


 Hexachlorobenzene
 Page 2
 October 1985

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Toxicity to Wildlife and Domestic Animals

     Bexaehlorobenzene WAS tested In several short-teen aquatic
bioassays, but no toxicity was observed at the Halt of solubility
of the compound.  Quail fed 20 ppra or sore of ICB in their
diets for 90 days had increased liver weights, and the size
and hatchability of their eggs decreased.  Feeding Kestrels
20 or 80 pp» HCB caused histological damage to both their livers
and kidneys.  Field studies of predatory and specifically fish-
eating birds showed some correlation between increased HCB
levels and increased mortality, low breeding success, and increased
porphyria.  However, other contaminants could also have been
responsible for these effects.

     Reduced reproductive success was observed in mink fed
1, 5, or 25 ppm of HCB in their diets (Bleavins et al. 1984).
Effects included decreased litter size, increased frequency
of still births, increased fetal mortality, and decreased post-
natal growth.


Regulations and Standards

Ambient Water Quality Criteria  (USEPA):

     Aquatic Life

     The available data are not adequate foe establishing criteria.

     Hunan Health

     Estimates of the carcinogenic risk associated with lifetime
     exposure to various concentrations of hezachlorobenzene
     in water are:

                                 Conce n t r a t i on

                                 7.2 ng/liter
                                 0.72 nf/liter
                                 0.07 ng/liter

GAG Unit Risk (USEPA):  1.67  (mg/kg/day)"1


REFERENCES
                        s
CASUAL, J.R.P., SHUBIK, P., MOLLNER, T. , and RAITAND, ?.  1977.
     Carcinogenic activity of heiachlorobenzene in hamsters.
     Nature 269:510-511
Hexachlorobenzene
Page 3
October 1985
                       313

-------
BLEAVINS, M.R., AtJLERlCH, R.J., tnd RINGER, U.K.  1984.  Effects
     of chronic dietary hexachlorobenzene exposure on the reprodue
     tive performance and survivabiiity of alnk and European
     ferrets.  Arch. Environ. Contaa. Toxicol. 13:357-365

COURTNEY, I.D.  1979.  Hexaehlorobenzene (HCB)»  A review.
     Environ. Res. 20:225-226

COURTNEY, K.D., COPELAND, M.F., and ROBBINS, A.  1976.  The
     effects of pentaehloronitrobenzene, hexachlorobenzene,
     and related compounds on fetal development.  Toxicol. Appl.
     Pharaacol. 35:239-256

GRANT, D.L., PHILLIPS, W.E.J., and HATINA, G.V.  1977.  Effect
     of hexachlorobenzene on reproduction in the rat.  Arch.
     Environ. Contaa. Toxicol. 5*207-216

IATROPOOLOS, M., HOBSON, W., KNAOF, V. , and ADAMS* H.  1976.
     Morphological effects of hexachlorobenzene toxicity in
     feaale rhesus monkeys.  Toxicol. Appl. Pharaacol. 37:433-444

INTERNATIONAL AGENCY FOR RESEARCH ON CANCER (ZARC).  LARC Mono-
     graphs on the Evaluation of Carcinogenic Risk of Chemicals
     to Humans.  Vol. 20t  Some Halogenated Hydrocarbons.
     World Health Organization, Lyon, franca

KHERA, K.s.  1974.  Teratogenicity and dominant lethal studies
     on hexachlorobenzene in rats.  Food Cosine t. Toxicol. 12:471-
     477

LYMAN, W.J., REEHL, W.P., and ROSENBLATT, D.B.  1982.  Handbook
     of Chemical Property Estimation Methods;  Environmental
     Behavior of Organic Compounds.  McGraw-Hill Book Co.,
     New York

O.S. ENVIRONMENTAL PROTECTION AGENOf (OSEPA).  1979.  Water-
     Related Environmental Fata of 129 Priority Pollutants.
     Washington, D.C,  December 1979.  EPA 440/4-79-029

U.S. ENVIRONMENTAL PROTECTION AGENCY (USEPA).  1980.  Ambient
     Water Quality Criteria for Chlorinated Benzenzes.  Office
     of Water Regulations and Standards, Criteria aad Standards
     Division, Washington, D.C."  October 1980.  SPA 440/5-80-028

U.S. ENVIRONMENTAL PROTECTION AGENCY {USEPA).  1984.  Health
     Iffacts Assessment for Hexachlorobenzene.  Environmental
     Crlteris and Assessment Office, Cincinnati, Ohio.  September
     1984.  ECAO-CIN-H017  (Final Draft)
Hexachlorobenzene
Page 4
October 1985
                                                                 J

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     Assessaent Document for Dichlorooethanc {Methylene Chloride),
     Office of Health and Environmental Assessment.  Washington,
     D.C.  February 1985.  EPA 600/8-82/004P

VZRSCHUEREN, X.  1977.  Handbook of Environaental Data on Organic
     Chemicala.  van Nostrand Reinhold Co., Hew York.  659 pages

WEAST, R.B., ed.  1981.  Handbook of Chemistry and Physics.
     62nd ed.  CRC Press, Cleveland, Ohio.  2,332 pages
Hexachlorobenzene
Page 5
October 1985

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                        HEXACHLOROBUTADIENE
 Summary
      Hexachlorobutadiene caused an increased incidence of kidney
 tumors in rats and was found to be rautagenic using the Ames assay.
 There Is equivocal evidence that hexachlorobutadiene increases
 neonatal mortality.  Chronic exposure to low levels of hexachloro-
 butadiene caused renal toxicity in rats and other studies have
 shown.that exposure can affect the central nervous system and liver.
 Hexachlorobutadiene is also quite toxic to aquatic organisms.
 CAS Numberi  87-68-3

 Chemical Formula:   C12C:CC1CC1:CC12

 IUPAC Kane:  Hexachloro-l,3-butadiene

 Important Synonyms and Trade Names:  Dolen, GP-40-66:120,  HCBD,
                                      perchlorobutadiene, C46


 Chemical and Physical Properties

 Molecular Weight!   260.74

 Boiling Point:   210 to 220*C

 Melting Points   -19 to -22«C

 Specific Gravity:   1.675 at 15.5«C

 Solubility in Waters  2 ag/liter at 20*C

 Solubility in Organicst  Compatible with numerous resins;  soluble
                          in alcohol and ether

 Log Octanol/Water  Partition Coefficients  4.8

 Vapor Pressure!  0.15 am Hg at 20*C
                          *w

 Transport and Fate

      Hexachlorobutadiene (HCBD)  is probably rather persistent
 in the environment.  Volatilization and adsorption to organic
 particulates are apparently important transport processes  for
 HCBD.  In soil and sediments, HCBD is bound to organic material.

 Hexachlorobutadiene
 Page 1
 October 1985


Preceding page blank

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 This  process  acts  as  a  sink  for HCBD  In  the  environment.  There
 was no  information on the  ultimate  fate  of HCBD  in  nature in
 the sources searched.


 Health  Effects

      The International  Agency  for Research on Cancer  (IARC  1979)
 notes that there is limited  evidence  that hexaehlorobutadiene
 is a  carcinogen.   Their conclusion  is based  on one  oral feeding
 study in rats in which  the Incidence  of  kidney tumors Increased
 in «h*e  animals  of  both  sexes given  the highest doses  (Xociba
 et al»  1977).   The results of  a spot  test of HCBD using the
 Ames  assay were positive.  The data on the reproductive toxlcity
 of HCBD are equivocal.   One  study indicates  that neonatal mor-
 tality  rose following a single, subcutaneous Injection of 20 mg/kg
 body  weight to  the dam  just  prior to  mating. Another, more
 recent  experiment  exposed  male and  female rats to doses of
 0.2,  2,  and 20  mg/kg/day for 90 days  prior to mating and 15
 days  during gestation;  no  toxic effects  were noted  in the off*
 spring.   However,  male  and female rats given 2 or 20 mg/kg/day
 of HCBD showed  signs  of renal  toxlcity.  The results of a 2-
 year  feeding  study in rats confirmed  that renal tubular hyper-
 plasia  was caused  by doses larger than 2 mg/kg/day.  Other
 studies have  indicated  that  HCBD also affects the central nervous
 system  and the  liver  (Harleman and  Seinen 1979).  HCBD is a
 cumulative toxin and  is therefore more toxic after  chronic
 exposures.  The oral to.,  for  adult rats is  250 ag/kg, and
 the I-DCQ  for  neonatal rats is  one-quarter that for  the adult
 animals.


 Toxiclty  to Wildlife  and Domestic Animals

     Hexachlorobutadiene is  very toxic to aquatic organisms,
 with  96-hour LC-Q  values for goldfish, rainbow trout, fathead
 minnow,  and blueglll ranging from 90  to  J30  Mg/liter.  Its
 chronic toxic!ty,  as measured  in an embryo-larval test in fathead
 minnows,  is ».3 ug/liter.  Invertebrates and saltwater fish
 were  affected at similar levels.

     The  ingeation of up to  30 ppm  of HCBD in their diets (approx-
 imately  5-f ag/kg)  had  no  effect on Japanese quail.

     Ho  studies on the  toxiclty on  HCBD  to domestic animals
 were discussed  In  the literature reviewed.


Regulations andStandards

Ambient Water Quality Criteria (USEPA)i
Hexachlorobutadiene
Page 2
October 1985

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           Aquatic Life
           The available data are not adequate for establishing criteria.

*\          Human Health
 1          Estimates of the carcinogenic risks associated with lifetime
           exposure to various concentrations of HCBD in water are:

           Risk                             Concentration

           10*1                             4.5 ug/litee
           10"?                             0.45 ug/liter
           10  '                             0.045 ug/liter

      CAG Unit Risk (USEPA)s  7.75xlO"2 (mg/kg/day)"1

      ACGIH Threshold Limit Value:  Suspected carcinogen 0.24 mg/m3  TWA

      REFERENCES

      AMERICAN CONFERENCE OF GOVERNMENTAL INDUSTRIAL HYGIENISTS (ACGIH).
           1980.  Documentation of the Threshold Limit Values.  4th
           ed.  Cincinnati, Ohio.  488 pages

      CHEMICAL DICTIONARY.  1977.  9th ed.  Hawley, G.G., ed.  Van
           Nostrand Reinhold, Co., New York

      HARLEMAN, J.H.,  and SEINER, W.  1979.  Short-term toxicity
           and reproduction studies in rats with hexaehloro-(1,3)-
           butadiene.   Toxicol. Appl. Pharmacol. 47:1-14

      INTERNATIONAL AGENCY FOR RESEARCH ON CANCER  (IARC).  1979.
           IARC Monographs on the Evaluation of the Carcinogenic
           Risk of Chemicals to Humans.  Vol. 20:  Some Halogenated
           Hydrocarbons.  World Health Organization, Lyon, Prance.
           Pp. 179-194

      KOCIBA, R.J., KEYES, D.G., JERSEY, G.C., BALLARD, J.J., DITTENBER,
           D.A., QUAST, J.P., WADE, C.E., HUMISTQH, C.G., and SCHWETZ,
           B.A.  1977.  Results of a two year chronic toxicity study
           with hexachlorobutadiene in rats.  Am. Ind. Hyg. Assoc.
           38:589-602

      NATIONAL INSTITUTE FOR OCCUPATIONAL SAFETY AMD HEALTH  (NIOSH).
           1984.  Registry of Toxic Effects of Chemical Substances.
           Data Base.   Washington, D.C.  October 19B4

      SCHWETZ, B.A., NORRIS, -?.M.f KOCIBA, R.J., KS1LSR, P.A., CORNIER,
           R.F., and GEHRING, P.J.  1974.  Reproduction study in
           Japanese quail fed hexachlorobutadiene for 90 days.  Toxicol.
           Appl. Pharmacol. 30:255-265

      SCHWETZ, 8.A., SMITH, F.A., HUMISTON, C.G., QUAST, J.F., and
           KOCIBA, R.J.  1977.  Results of a reproduction study in

      Hexachlorobutadiene
      Page 3
      October 1985
                                                      ^
                                                        D*m*nt AMOCIBCM

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     rats fed diets containing hexachlorobutadiene.  Toilcol.
     Appl. Pharaacol. 42:387-398

U.S. ENVIRONMENTAL PROTECTION AGENCY (OSEPA).  1979.  Water-
     Related Environmental Fate of 129 Priority Pollutants.
     Washington, D.C.  December 1979.  1PA 440/4-79-029

U.S. ENVIRONMENTAL PROTECTION AGENCY (USEPA).  1980.  Ambient
     Water Quality Criteria for Bexaehlorobutadiene.  Office
     of Water Regulations and Standards, Criteria and Standards
     Division, Washington, D.C.  October 1980.  EPA 440/5-80-053

U.S. ENVIRONMENTAL PROTECTION AGENCY (USBPAJ.  1984.  Health
     Effects Assessment for Bexaehlorobutadiene.  Environmental
     Criteria and Assessment Office, Cincinnati, Ohio.   September
     1984.  ECAO-CIN-I053  (Final DraftI

U.S. ENVIRONMENTAL PROTECTION AGENCY (USEPA).  198S.  Health
     Assessment Document for Dichlorometnane  (Methylene Chloride).
     Office of Health and Environmental Assessment.  Washington,
     D.C,  February 1985.  SPA 600/8-82/OQ4P

WEAST, R.E., ed.  1981.  Handbook of Chemistry and Physics.
     62nd ed.  CRC Press, Cleveland, Ohio.  2,332 pages
Hexachlorobutadiene
Page 4
October 198S
                               £20

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                      HEXACHLOROCYCLOHEXANE
Summary

     Hexachlorocyclohexane  (HCH) has four major isoraers, alpha,
beta, gamma, and delta, of which the gamma isomer  (lindane) is
generally the most active.  HCH 'is- fairly persistent in the en-
vironment.  Three of the isomers caused liver tumors in mice
when administered alone.  Exposure to lindane decreased the num-
ber of. live young produced by pregnant dogs.  Lindane is also
quite"" toxic to aquatic life.
Note;  Information presented below should be considered gener-
ally applicable to the HCH isoners unless a specific isomer is
indicated.
CAS Kumber:  608-73-1
             alpha-HCHi  319-84-6
             beta-HCH{  319-85-7
             gamma-HCH:  58-89-9
             delta-HCH!  319-86-8

Chemical Formula:  CgHgClfi

IUPAC Name:  1,2,3,4,5,6-Hexachlorocyclohexane

Important Synonyms and Trade Names:  Benzene hexachloride, HCH,
                                     Lindane {gamma-HCH), HCH


Chemical and Physical Properties

Molecular Weight!  290.82

Boiling points  No available data

Melting Point:  alpha-BCH:  158-C
                beta-HCHi  310*C
                gamsBa-HCHi  112 °C
                delta-HCH*  138«C
                Technical HCH: 65°C
                         s,
Solubility ia Waters  alpha-HCH:  10 ag/liter
                      beta-HCH:  5 ng/llter
                      gamma-HCH:  10 tag/liter
                      delta-HCH:  10 mg/liter
                      Technical HCHt  10-32 ag/liter
HexachLorocyclohexane
Page 1
October 1985
                                                         mmocmtm*

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 Log Oetanol/Water  Partition Coefficient!  3.8

 Vapor Praa»ur«t  alpha-HCHr   2.5  x  10l5 mm Eg  at 20*C
                 beta-HCH:  2.8 x 10~7 mm Hg at 20 »C
                 gamma-HCHt   2 x  10"* mm Hg at 20 «C
                 delta-ICHt   1.7  x  10" 3 mm Hg  at 20 »C


 Transport  and Fata

   ..-.-In general, the  transport and  fats of the hexachlorocyclo-
 hexane isomers is  similar and they  will therefore be discussed
 as a group.  The primary transport  and fate process for  hexa-
 chlorocyclohexane  in  an aqueous system appears to be adsorption
 to organic particles, transport to  anaerobic sediments,  and
 subsequent biodegradation by  anaerobic organisms.  Volatilization
 nay be somewhat important in  the  aquatic environment and  is
 probably a major transport process  in soils.   It is important
 to note that biodegradation of hexachlorocyclohexane yields
 such chemicals as  pentachlorocyclohexane, tetrachlorobenzene,
 and trichlorophenol and therefore may not result in substantial
 detoxification of  the chemical.   Lindane has been shown  to be
 rather persistent  when applied to soil, with up to 10 percent
 of an applied sample  remaining after 10 years.


 Health Effects

     The alpha, beta* and gamma isomers of hexachlorocyclohexane
 have all been shown to cause  liver  tumors in mice but not in
 other tested species.  BCH has not  been thoroughly tested for
 genotoxic  effects  but does not appear to be autagenic.  The
 alpha, beta, and delta isomers have not been tested for  their
 teratogenic or reproductive toxicological potential.  Lindane
 has been tested and was not teratogenic, but in two studies it
 decreased  the- number  of live  young  produced (Earl et al.  1973).
 Alpha-HCH  has been shown to cause nonmalignant lesions in the
 liver of test animals at doses below those required to induce
 tumors.  Lindane has  been associated with the  development of
 aplastlc anemia in humans (West 1967}.


 Toxicity to Wildlife  and Domestic Animals

     Lindane (ganraa-HCH) is responsible for the effectiveness
 of hexachlorocyclohexane as an insecticide and is generally
more toxic than the other Isomers or technical HCB.  In  fact,
 the presence of the other HCH isomers decreases the toxlcity
of llndane to aquatic organisms,  either by an  antagonistic
effect or  by decreasing the chemical*• solubility.  Therefore,
 the toxiclty of lindane and HCH will be considered separately.
Hexachlorocyclohexane
Page 2
October 1985

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     Lindane Is acutely toxic to freshwater fish with LC_Q
values ranging fron 2 pg/liter to 141 pg/liter; and to silt-
water fish at levels of from 7.3 to 104 yg/liter.  Lindane
was acutely toxic to the pink shrimp at 0.17 yg/liter.  Acute-
chronic ratios foe llndane ranged from 7.5 to 63, and therefore
the Final Chronic Value for the protection of freshwater species
was determined to be 0.08 Mg/liter.  Aquatic organisas appear
to bioconcentrate between 100 and 500 tines the steady-state
concentration of lindane in the water.

     Technical hexachlorocyclohexane was much less toxic than
lindane, with acute toxicity ranging from 100 pg/liter to 15,000
Mg/liter for freshwater fish.  Data on saltwater species also
indicated that the technical compound was less acutely toxic.
Ho information was available on the chronic toxicity of HCH.
A bioconcentration factor was not reported but is probably
similar to that for lindane.

     NO studies on the toxicity of the HCH isomers to terres-
trial or domestic animals was found in the literature reviewed.
Howeverr voles at Love Canal that had decreased lifespans and
reproductive ability had high levels of lindane in their livers
(Rowley et al. 1983).


Regulations and Standards

Ambient Water Quality Criteria (DSEPA):

     Aquatic Life

     Hexachlorocyclohexane mixture:

     The available data are inadequate for establishing final
     criteria for hexachlorocyclohexane mixture.  However,
     EPA did report the lowest values known to cause toxicity
     in aquatic organisas.

     Freshwater

         Acute toxicityj  100 pg/liter
         Chronic toxicity:  80 available data

     Saltwater

         Acute toxicity:  0.34 Mg/liter
         Chronic toxicity:  Mo available data
Hexachlorocyclohexane
Page 3
October 1985
                        323

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     L ind ana  (g amma-HCH ) :

     Freshwater
                toxicity!  2.0 ug/liter
         Chronic toxicity t  0.08 pg/liter

     Saltwater

         Acute  toxicity:  0.16 pg/liter
         Chronic toxicityi  No available data

     Human Health

     Estimates  of the carcinogenic risks associated with lifetime
     exposure to various concentrations of the HCH isomers
     in water are:
           Alpha-HCl
         Concentration

         92 ng/lit«r
         9.2 ng/liter
         0.92 ng/liter
                           Beta-BCH
                         Cone e n t r a t i on

                         163 ng/liter
                         16.3 ng/liter
                         1.63 ng/liter
  Gamma-HCH
Concentration

106 ng/liter
18.6 ng/liter
1.86 ng/liter
Technical I
Concentrat:

123 ng/lit.
12.3 ng/lii
1.23 ng/lii
Interim Primary Drinking Water Regulation:  gamma-HCH:

CAG Uni t Risk  '**e«n* t .  mt •>« «_as*a .  1^1  iimr* /tm /J •«. v — •*
                                                        0.004 mg/lit
               (USEPA)s  alpha-HCHs   11.1  (ag/kg/dayT
                        beta-aCH:   1.84  (ag/kg/day  *  .
                        gaama-HCHi   1.33  
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NATIONAL CANCER INSTITUTE  (NCI).  1977.  iioassay of Lindane
     for Possible Carcinogenicity.  CAS No. 58-89-9.  NCI Car-
     cinogenesis Technical Report Series No. 14*  Washington,
     D.C.  DHEW Publication No.  (NIOSH) 77-814 .

NATIONAL INSTITUTE FOR OCCUPATIONAL SAFETY AND HEALTH (NIOSH).
     1983*  Rtgistry of Toxic Effects of Chemical Substances.
     Data Base.  Washington, D.C.  October 1983

ROWLEY, M.H., CHRISTIAN, J.J., BASA, O.K., PAWLIKOWSKI,  M.A.,
     and PAIGEN, B.  1983.  Use of snail mammals (voles) to
     assess a hazardous waste site at Love Canal, Niagara Falls,
     New York.  Arch. Environ. Contain. Toxicol. 12:383-397

U.S. ENVIRONMENTAL PROTECTION AGENCY  (USEPA).  1979.  Water-
     Related Environmental Fate of 129 Priority Pollutants.
     Washington, D.C.  December 1979.  EPA 440/4-79-029

U.S. ENVIRONMENTAL PROTECTION AGENCY  (USEPA).  1980.  Ambient
     Water Quality Criteria for Hexachlorocyclohexane.  Office
     of Water Regulations and Standards, Criteria and Standards
     Division, Washington, D.C.  October 1980.  EPA 440/5-80-054

U.S. ENVIRONMENTAL PROTECTION AGENCY  (USEPA) .  1984.  Health
     Effects Assessment for Lindane.  Environmental Criteria
     and Assessaent Office, Cincinnati, Ohio.   September 1984.
     ECAO-CIN-H056  (Final Draft)

U.S. ENVIRONMENTAL PROTECTION AGENCY  (USEPA).  1985.  Health
     Assessment Document Cor Dichloromethane (Methylene Chloride).
     Office of Health and Environmental Assessment.  Washington,
     D.C.  February 1985.  EPA 600/8-82/004F

VERSCBUEREN, K.  1977.  Handbook of Environmental Data on Organic
     Chemicals.  Van Nostrand Relnhold Co., New York.  €59 pages

WEAST, R.E., ed.  1981.  Handbook of Chemistry and Physics.
     62nd ed.  CRC Press, Cleveland, Ohio.  2,332 pages

WEST, I.  1967.  Lindane and heaatologic reactions.  Arch.
     Environ. Health 15i97-101
Hexachlorocyclohexane
Page 5
October 1985

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                          HEXACHLQROETHAHE
  Summary
       Hexachloroethane produced liver tumors in nice when admini-
  stered by gavage.  it caused central nervous aytern effects,
  hepatic dysfunction; and renal damage at high doses in animal
  studies.
  CAS Numbers  67-72-1

  Chemical Formula;  C2Clg

  I UP AC Name:  Hexachloroethane

  Important Synonyms and Trade Harness  Ethylene hexachloride,
                                     .  hexachloroethylene, carbon
                                       hexachloride


  Chemical and Physical properties

  Molecular Weight:  237

  Boiling Points  1S?*C (sublimes)

  Melting Points  187'C (sublimes)

  Specific Gravltys  2.09
                   .-.
  Solubility in waters  50 mf/liter

  Solubility in Organics:  Soluble in alcohol, benzene, chloroform
                           and ether

  Log Octanol/Water Partition Coefficients  3.34

  Vapor Pressures  0.4 mm Eg at 20 *C
  Transport &n4j Fate

       Hexachloroethane is "relatively persistent in the environ-
  ment.  Volatilization may be an important transport process
  but probably occurs slowly from natural waters.  Hexachloroethane 's
  high log octanol/water partition coefficient suggests that
  it adsorbs to organics in the soil and sediment and that it
  may bioaccumulate.  Biodegradation is unlikely to be a signif-
  icant fate process.


  Hexachloroethane
  page 1
  October  1985
Preceding page blank

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Health Effects

     Thert is limited evidence that hexachloroethane is carcino-
genic in experimental animals.  In a National Cancer Institute
study, hexachloroethane administered by gavage produced malignant
liver tumors in male and female B6C3P1 mice.  It did not cause
a statistically significant increase in tumors in Osborne-Mendel
rats, but some rare renal tumors did develop.  Hexachloroethane
has not been reported to be mutagenic.  Reduced litter sizes
were..observed after oral administration of 5,500 mg/kg to preg-
nant rats.
             *

     Hexachloroethane"s major physiological effect in animals
is on the central nervous system.  Oral doses of 1-1.4 g/kg
caused weakness, staggering gait, and twitching muscles in
dogs.  Hepatic dysfunction and renal damage were also reported
in various experiments.  The oral LD.Q for rats was 4,460 nig/kg.
The dermal LD5Q for rabbits was more^than 32,000 mg/kg.


Toxlclty to Wildlife and Domestic Animals

     Hexachloroethane is stored in animals' fat, and some bio*
accumulation would be expected in animals higher on the food
chain.

     The 48-hour I.C.Q for Daphia magna is 8/070 uf/liter; the
48-hour LC.rt for thi larva of the midge, Tanytarus dissimilis,
is 1,700 n|/liter.  Th« 96-hour, static 1C-, is 980 Mf/liter
for both the bluegill and the rainbow trout, and it is 2,400 ug/litti
for the sheepshead minnow.  In embryo-larval ttsts on the fathead
minnow, the chronic toxicity value was reported to be 540
Regulations and Standards

Ambient Water Quality Criteria  (USEM) *

     Aquatic Life

     The available data are not adequate for establishing criteria

     Human Health

     Estimates of the carcinogenic risks associated with lifetime
     exposure to various concentrations of hexachloroethane
     in water arei

                                 Concentration

                                 19 uf/litsr
                                 1.9 pg/liter
                                 0.19 ug/littr

Hexachloroethane
Page 2
October 1985
                                                                   -

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GAG Unit li§k  (USEPA) s   1.4xlO~2  (mg/kg/day)'1

OSHA Standard  (skin)t  10 mg/n3 TWA

ACGIH Threshold Liait Value:  100 mg/m3 TWA


REFERENCES

AMERICAN CONFERENCE OF GOVERNMENTAL INDUSTRIAL HYGIENISTS (ACGIH}
     1980.  Documentation of the Threshold Liait Values.  4th
     ed.  Cincinnati, Ohio.  488 pages

INTERNATIONAL AGENCY FOR RESEARCH ON CANCER (IARC).  1979.
     IARC Monographs on  the Evaluation of the Carcinogenic
     Risk of Chemicals to Humana.  Vol. 20:  Some Halogenated
     Hydrocarbons.  World Health Organization, Lyon, France.
     Pp. 241-257

THE MERCK INDEX.  1976.  9th ed.  Windholz, M., ed.  Merck
     and Co., Rahway, New Jersey

NATIONAL CANCER INSTITUTE (NCI).  1978.  Bioassay of hexachloro-
     ethane for Possible Carcinogenicity.  (CAS No. 67-72-1)
     NCI Careinogenesis Technical Report Series No. 68.  wash*
     ington, D.C.  DHEW publication No. (NIB)  78-1318

NATIONAL INSTITUTE FOR OCCUPATIONAL SAFETY AND HEALTH  (NIOSB).
     1984.  Registry of Toxic Effects of Chemical Substances.
     Data Base,  Washington, D.C.  October 1984

U.S. ENVIRONMENTAL PROTECTION AGENCY (USEPA).   1979.  Water-
     Related Environmental Fate of 129 Priority Pollutants.
     Washington, D.C,  December 1979.  EPA 440/4-79-029

U.S. ENVIRONMENTAL PROTECTION AGENCY (USEPA).   1980.  Ambient
     water Quality Criteria for Chlorinated Ethanes.  Office
     of Water Regulations and Standards, Criteria and Standards
     Division, Washington, D.C.  October 1980.  EPA 440/5-80-029

U.S. ENVIRONMENTAL PROTECTION AGENCY (USEPA).   1985.  Health
     Assessment Docuaent for Dichloronethane (Methylene Chloride).
     Office of Health and Environmental Assessment.  Washington,
     D.C,  February 1985.  EPA 600/8-82/004?

VERSCHUEREN, X.  1977.  Handbook of Environmental Data on Organic
     Chemicals.  Van Nostrand Reinhold Co., New York.  659 pages

MEAST,  R.E., ed.  1981.  Handbook of Chemistry and Physics.
     62nd ed.  CRC Press, Cleveland, Ohio.  2,332 pages
Hexachloroe thane
Page 3
October 1985
                       32 <*

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                            HEXACHLOROPHENE
   Summary
        lexachlorophene severely damages  neonates1  central  nervous
   systems.   It has had teratogenic  and reproductive  effects  in
   animals.   There is suggestive evidence that  hexachlorophene
   is also teratogenic in humans.


   CAS Number:   70-30-4

   Chemical  Formula:   (CgHCl3OB) 2CH2

   I UP AC Name:   2,2-Methylene-bis(3, 4, 6-trichlorophenol)

   Important Synonyms and Trade  Names:  Hexide, Nabac


   Chem ical  and Physical Properties

   Molecular Weight:   406,9

   Boiling Point:   No available  data

   Melting Point;   165«C

   Specific  Gravity:   No available data

   Solubility in Water:  Practically insoluble  in water;  estimated
                         to  be 50 mg/liter

   Solubility in Organica:   Soluble  In acetone/ alcohol,  ether,
                            and  chloroform

   Log Octanol/Hater  Partition Coefficient:   3.93

   Vapor Pressure:  Estimated to* be  10**  mm Eg  at 20*C


   Transport and Pate

        Mo information on the transport and fate of hexachlorophene
   was found in the sources  reviewed.  Its water solubility and
   vapor pressure  suggest that it would not be  very volatile.
   Its high  log octanol/water partition coefficient indicates
   that it is likely  to be adsorbed  to soil and sediments.  Hexa-
   chlorophene  is  not degraded by laboratory  animals.  Therefore,
   bioaccumulation, and subsequent degradation, is  unlikely to
   be  an important fate.  Hexachlorophene is  probably persistent
   in  the environment.
  Hexachlorophene
  Page  1
  October  1985
Preceding page blank
                         331

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Health Effects

     In the 1960s, soap containing hexachlorophene was used
to bathe neonates in hospital nurseries.  Some of the infants
developed symptoms of central nervous system damage/ with twitch-
ing, convulsions, and death.  The neurological damage, especially
of the white matter of the cerebrum and brainstea, was severe.
In animal studies, it has been shown that treatment with hexa-
ehlorophene inhibited the synthesis of ayelln in the peripheral
and central nervous systems.

     Hexachlorophene was not carcinogenic in an NCI study in rats
(IARC 1979).  A series of in vivo and in vitro mutagenesis assays
did not yield positive results.  There is some evidence that a
higher incidence of malformations among the children of hospital
workers is due to repeated hexachlorophene exposure.  Pregnant
rats administered hexachlorophene in their diets or by gavage had
smaller litters and an increased incidence of cleft palate and
other fetal abnormalities.  The oral LD5Q of hexachlorophene
is 60 rag/Kg for both the rat and the guinea pig, and 67 ng/kg
for the mouse.  The dermal LD.. values are 1,840 ng/kg, 1,100 ag/kg,
and 270 mg/kg, for the rat, guinea pig, and mouse, respectively.


Toxicity to Wildlife and Domestic Animals

     No information on the toxicity of hexachlorophene to wild-
life and domestic animals was available in the sources reviewed.


Regulations and Standards

     No regulations or standards have been established for
hexachlorophene.


REFERENCES                •  ,

DOULL, J., KLAASSEN, C.D., and AMDUR, M.O., eds.  1980.  Casarett
     and Doull's Toxicology:  The Basic Science of Poisons.
     2nd ed.  Macmillan publishing Co., New York.  778 pages

OILMAN, A.G., GOODMAN, L.S., AND OILMAN, D.  1980.  Pharmaceu-
     tical Basis of Therapeutics.  6th ed.  Macmillan Publishing
     Co.,  New fork
                        v
INTERNATIONAL AGENCY FOR RESEARCH ON CANCER (IARC).  1979.
     IARC Monographs on the Evaluation of the Carcinogenic
     Risk of Chemicals to Buaans.  vol. 20:  Some lalogenated
     Hydrocarbons.  World Health Organization, Lyon, France.
     Pp. 241-257
Hexachlorophene
Page 2
October 1985
                                                                   ;
                                                                   jt

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LYMAN, W.J., REEHL, W.F.» ftfid ROSENBLATT, D.H.  1982.  Handbook
     of Chemical Property Estimation Methods:  Environmental
     Behavior of Organic Compounds.  McGraw-Hill Book Co.,
     New York

THE MERCK INDEX.  1976.  9th ed.  Windholz, M., ed.  Merck
     and Co., Rahway, Hew Jersey

NATIONAL CANCER INSTITUTE (NCI).  1978.  Bioassay of Hexachloro-
     phene for Possible Carcinogenicity.  (CAS No.70-30-4)
     NCI Carcinogenesis Technical Report Series No. 40.  Washing-
     ton, B.C.  DHEW Publication No. (NIB)  78-840

NATIONAL INSTITUTE FOR OCCUPATIONAL SAFETY AND HEALTH (NIOSH).
     1984.  Registry of Toxic Effects' of Chemical Substances.
     Data Base.  Washington, D.C.  October 1984

SAX, N.I.  1975.  Dangerous Properties of Industrial Materials.
     4th ed.  Van Nostrand Reinhold Co., New York.  1,218 pages

VERSCHUEREN, x.  1977.  Handbook of Environmental Data on Organic
     Chemicals,  van Nostrand Reinhold Co., New York.  8S9 pages

WE AST, R.E., ed.  1981.  Handbook of Chemistry and Physics.
     62nd ed.  CRC Press, Cleveland, Ohio.  2,332 pages
Hexachlorophene
Page 3
October 1985
                                                     «ne Ammocmtmm

                      333

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                              HEXANE
Summary
     Fetotoxicity was produced by the administration of hexane
to pregnant rats.  In humans, hexane Irritates the amcous membranes
eyes, and skin and can cause dermatitis and pulmonary edema.
Chronic exposure to hexane can cause polyneuropathy with axonal
degeneration of the peripheral nervous system.
CAS Number:  110-54-3
Chemical Formula:  C,H,t
                    o 14
IUPAC Name:  n-Hexane
Important Synonyms and Trade Names:  n-Hexane, hexyl hydride

Chemical and Physical Properties
Molecular Weight:  86.20
Boiling Point:  68.9*C
Melting Point;  -I4*C
Specific Gravityt  0.6603 at 2Q«C
Solubility in Water:  140 mg/liter at 20«C
Solubility In Organics:  Soluble In alcohol and ether
Log Octanol/Water Partition Coefficient:  4.3 (calculated)
Vapor Pressure:  124 mm Eg at 20*C
Vapor Density;  3.0
Flash Point:  -21.7*C (closed cup)

Tr ansport^and Fate
                        ^
     Hexane volatilizes readily from surface water and reacts
with OH radicals in the air.  In the soil, It is partially
adsorbed to the surface of organic materials but may leach
into the groundwater.
Bexane
Page 1
October 1985
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Health Effects

     Hexant did not promote tumors when it was administered
to mice topically and subcutaneously.  NO other data on the
earcinogenieity of hexane were found  (Kraeaer et al. If74).
There were no mutagenicity data available in the literature
surveyed.

    .Pregnant Fischer 344 rats were exposed to 1,000 ppn  (3,600
mg/m ) of hexane for 6 hours on the 20th day of gestation.
Significant amounts of hexane and the neurotoxic metabolite
2,5-hexanedione Appeared in the fetal tissues (Bus et al. un-
dated) .  fetotoxicity was observed in mice when pregnant  females
were given oral doses of 238 ag/kg froa the 6th to 15th days
of gestation.  No evidence of teratogenicity was reported in
the literature reviewed.

     In humans, aild exposure to hexane vapors can irritate
the mucous membranes.  Exposure to air concentrations greater
than It hexane nay cause dizziness, unconsciousness, and death.
Direct skin contact causes irritation and dtraatitis.  Inhalation
exposure can cause chemical pneuaonitus, pulmonary edema,,and
hemorrhage.  Exposure to levels of 5,000 ppn (18,000 mg/m )
for 10 minutes reportedly caused dizziness, and exposure  to
5,400 mg/m  caused nausea, and eye and throat irritation.

     Chronic exposure to hexane causes polyneuropathy with
axonal degeneration of the distal parts of the peripheral nervous
systen, as well as the spinal cord and brain sten.  Resulting
afflictions are weakness, memory loss, nuabness, and headaches.
Yamaraura (1969) described peripheral nervous systen disturbances
in 93 workers at a sandal manufacturing facility in Japan where
hexane concentrations ranged from 1,800 to 9,000 mg/m .  The
oral LD5« for rats is reported to be 287 ag/kg.

     A chronic oral study in which rats were given 400-600 tag/liter
hexane in water per day  (approximately 100-150 ag/kg/day) for
5 months resulted in peripheral neuropathy and distal nerve fiber
degeneration.  Repetitive subcutaneous injections or inhalation
also produced peripheral neuropathy (Spenser and Schaumburg
1977).


Toxicitv to Wildlife and Domestic Animals
                       \
     No Mortalities were reported aaong young Coho aalaon exposed
to 100 »f/liter hexane for 96 hours in sea water.
lexane
Page 2
October 19SS

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Regulations and Standards

OSHA Standardt  1,800 ng/m3 TWA

ACGIH Threshold Limit Value:  180 ag/m3,TWA (n-hexane)
                              1800 mg/m  TWA (other iionera}


REFERENCES

AMERICAN CONFERENCE OF GOVERNMENTAL INDUSTRIAL HYGIENISTS (ACGIH).
     1980.  Documentation of the Threshold Limit Values.  4th ed.
     Cincinnati* Ohio.  488 pages

ANONYMOUS.  1958.  Environmental hydrocarbons produce degenera-
     tion in cat hypothalamus and optic tract.  Science 119:199

BUS, J.S., WHITE, Z.L., HECK, H.A., and GIBSON, J.E.  Undated.
     The distribution and metabolism of n-hexane in pregnant
     Fischer 344 rats.  Chemical Industry Institute of Toxicology,
     Research Triangle Park* North Carolina

KIRK-OTHMER ENCYCLOPEDIA OF CHEMICAL TECHNOLOGY.  1980.  3rd ed.
     Grayson, M.I ed.  Vol. 12, p. 929

KRAEMER, A., STANDINGER, H., and ULLRICH, V.  1974.  Effects
     of n-hexane inhalation on the mono oxygenase system in
     nice livec microsomes.  Chen. Biol. Interactions 8:11*18

NATIONAL INSTITUTE FOR OCCUPATIONAL SAFETY AND HEALTH (HIOSH).
     1983.  Registry of Toxic Effects of Chemical Substances.
     Data Base.  Washington, D.C.  October 1983

PAULSON, G.W., and WAYLONIS, G.W.  1976.  Pol/neuropathy due
     to n-hexane.  Arch. Intern, Med.  136:880-882

SCHAUMBURG, H.H., and SPENSER, P.S.  1976.  Degeneration in
     central and peripheral* nervous systems produced by pure
     n-hexane, an experimental study.  Brain 99:183-192

SPENSER, P.S., and SCHADMBORG, H.H.  1977.  Proc. R. Soc. Med.
     70i37-39

VERSCHUERIN, 1.  1977.  Handbook of Environmental Data on Organic
     Chemicals.  Van Nostrand leinhold Co., New York.  659 pages

WEAST, R.E., ed.  1981.  Handbook of Chemistry and Physics.
     62nd ed.  CRC Press, Cleveland, Ohio.  2,332 pages

YAMAMURA, Y.  1969.  n-Bexane polyneuropathy.  Japonica, 23(1).
Hexane
Page 3
October 1985
'i 'i 1
                                                        Ammeem

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                                 IRON
  Summary
       There is tone evidence that high concentrations of certain
  soluble icon salts nay be teratogenic.  The ingestion of excess
  amounts of iron can irritate the gastrointestinal tract*  Inhaling
  some iron-containing dusts and fumes can cause siderosis, a
  type of benign pneumoconiosis.


  Background Information

       Iron is the fourth aost abundant element in the earth's
  crust.  The pure metal is very reactive chemically,  it corrodes
  readily in the presence of oxygen and moisture, forming iron
  (III) hydroxide [Fe(OH)3].

  CAS Number:  7439-89-6

  Chemical Formula;   Pe


  Chemical and Physical Properties

  Atomic Weights  55.847

  Boiling Point:  2,7SQ»C

  Melting Point:  lf535*C

  Specific Gravity:   7.86

  Solubility in Water:  Insoluble

  Solubility in Organics:  Soluble in alcohol and ether


  Transport and Pate

       Elemental iron and many iron compounds, including Fe(OH),
  and the iron oxides, are insoluble in water.  Iron also tends
  to chelate with organic and inorganic matter.  Consequently,
  much of the iron present in aquatic systems tends to partition
  into the bottom sediments.  Iron has relatively low mobility
  in soil.  Atmospheric transport of iron can occur.
  Iron
  Page 1
  October 1985
Preceding page blank

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Health Effects

     Some studies have Indicated that inhalation exposure to
high concentrations of iron oxide is associated with increased
risk of lung and laryngeal cancers in hematite miners and foundry
workers.  Bowever, the significance of these findings is not
established since exposures were to a mixture of substances,
including radon gas and decomposition products of synthetic
resins.  Iron dextran solutions are reported to cause injection
site sarcomas in experimental animals.  Some iron compounds,
notably ferrous sulfate, are reported to have high mutagenic
activity in test systems.  Intravenous injection of high con-
centrations of soluble iron salts is reported to cause terato-
genic effects, including hydrocephalus and anophthalmia, in
various species of experimental animals.

     Iron is an essential element in plants and animals.  Bow-
ever, the ingestion of excess amounts of iron produces toxic
effects, primarily associated with gastrointestinal irritation.
Severe poisoning may cause gastrointestinal bleeding, pneumo-
nitis, convulsions, and hepatic toxicity.  A dose of about
30 g of a soluble ferric salt is likely to be fatal in humans.
Persons ingesting more than 30 mg/kg should be observed for
clinical symptoms and possibly hospitalized.  Chronic ingestion
of excess iron may lead to hemosiderosis or hemochromatosis.
Long-term inhalation exposure to iron-containing dusts and
fumes, especially iron oxide, can produce siderosis.  This
condition is considered to be a type of benign pneuatoconiosis
that does not progress to fibrosis.  Exposure to aerosols and
mists of soluble iron salts may produce respiratory and skin
irritation.  The toxic effects of iron in experimental animals
are similar to those observed in humans.


Toxicity to Wildlife and Domestic Animals

     The available data are not adequate to characterize the
toxicity of iron to wildlife or domestic animals.  Iron is
unlikely to cause ecological toxicity.


Regulations and Standards

OSHA standards  10 ag/a3 TWA (iron oxide fuse)

ACGIH Threshold Limit Valuesi

     5 mg/m -TWA (iron oxide fume, as fe)
     10 mg/m  STEL  (iron oxide fume, as re)
     1 mg/m:: TWA  (soluble iron salts, as Fe)
     2 mg/m* STEL (soluble iron salts, as Ft)
Iron
Page 2
October 1985

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REFERENCES

AMERICAN CONFERENCE OF GOVERNMENTAL INDUSTRIAL HYGIENISTS (ACGIH),
     1980.  Documentation of the Threshold Limit Values.  4th ed.
     Cincinnati, Ohio.  488 pages

DOULL, J.» KLAASSEN, C.D., and AMDOR, M.O.  1980.  Casarett
     and Doull's Toxicology:  The Basic Science of poisons.
     2nd ed.  Macmillan Publishing Company, New York.   778
     pages

NATIONAL INSTITUTE FOR OCCUPATIONAL SAFETY AND HEALTH  (NIQSH).
     1984.  Registry of Toxic Effects of Chemical Substances.
     Data Base.  Washington, D.C.

NATIONAL RESEARCH COUNCIL.  1982.  Diet, Nutrition, and Cancer.
     National Academy Press, Washington, D.C.

U.S. ENVIRONMENTAL PROTECTION AGENCY (USEPA).  1984.  Health
     Effects Assessment for Iron.  Environmental Criteria and
     Assessment Office, Cincinnati, Ohio.  September 1984.
     ECAO-CIN-H054  (Final Draft)

WEAST, R.E., ed.  1981.  Handbook of Chemistry and Physics.
     62nd ed.  CRC Press, Cleveland, Ohio.  2332 pages
Iron
Page 3
October 1985
                      3HI

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                            ISOBUTYL ALCOHOL
    Summary
         Rats injected subcutaneously with isobutyl alcohol developed
    liver and gastrointestinal tumors.  At high concentrations,
    it depresses the central nervous system and irritates the skin,
    eyes and throat in both animals and humans.  High concentrations
    of isobutyl alcohol have also been shown to cause slight changes
    in the liver and kidneys of exposed mice.


    CAS number:  78-83-1

    Chemical Formula:  CH3CHCH3CI2OH

    IUPAC Name:  2-Methyl propanol

    Important Synonyms and Trade Hamest  Isobutanol


    Chemical and Physical Properties

    Molecular Weight:  74

    Boiling Point:   1QS*C

    Melting Points   -1Q8«C

    Specific Gravity:  0.805 at 20*C

    Solubility in Waters  95,000 mg/liter at 18*C

    Solubility in Organics:  Soluble in alcohol and ether

    Log Octanol/Water Partition Coefficient:  1.0 (calculated)


    Transport and Fata

         No information on the transport and fate of isobutyl alcohol
    was found in the sources reviewed.  However, likely transport
    and fat* processes can be determined based on the general reac-
    tions of alcohols and the specific chemical and physical prop-
    erties of this  material.

         Alcohols aft very soluble in water and therefore probably
    are not very volatile, although some evaporation may occur.
    Oxidation is likely to be an important fate process in both
    surface water and the atmosphere.  In soil, isobutyl alcohol
    is probably biodegraded by soil microorganisms.


    Isobutyl alcohol
    Page 1
    October 1985

                                                   C

Preceding page blank  ,

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Health Effects

     Although the evidence on whether iaobutyl alcohol is a
tumorigenic agent when administered orally in rats is equivocal,
this compound is carcinogenic when injected subcutaneouslyr
producing liver and gastrointestinal tumors.  Isobutyl alcohol
reportedly causes mutations in Bscheriehia eoli strain A and
cytogenic effects In Saccharomyces cerevisiae7~ Ho reproductive
or teratogenic effects have been reported.

     Zsobutyl alcohol at high concentrations depresses the
central nervous system in both animals and man.  Other symptoms
of excessive exposure are irritation of the eye and throat/
formation of vacuoles in the superficial layers of the cornea,
and loss of appetite.  Direct application of isobutyl alcohol
irritates the skin, causing erythemia and hyperemia.  A dose
of It,370 mg/mj inhaled for 13$ hours has a narcotic effect
in nice and causes slight changes in the liver and kidneys.
The oral LD«.n for rats is 2.46 g/kg, while the dermal LD-n
for rabbits3!* 4.21 g/kg.                               50


Toxlcity to Wildlife and Domestic Animals

     Limited information is available on the effects of isobutyl
alcohol on the environment.  Inhibition of cell division occurs
at 280 rag/liter for the bacterium PseudomonaspatIda and at
290 mg/liter for the alga Micrpcystis aerugi nosa«


Regulations and Standards

OSHA Standard (air):  300 mg/m3 TWA

ACGIH Threshold Limit values;  150 mg/m!  TWA
                               225 mg/mj STBL
REFERENCES

AMERICAN CONFERENCE OF GOVERNMENTAL INDUSTRIAL H7GIENISTS (ACGIH)
     1980.  Documentation of the Threshold Limit Values.  4th
     ed.  Cincinnati, Ohio.  488 pages

LYHAN, W.J., REEHL, W.P., and ROSENBLATT, D.H.  1982.  Handbook
     of Chemical Property Estimation Methods:  Environmental
     Behavior of Organic Compounds.  McGraw-Hill Book Co.,
     New fork

TH MERCK INDEX.  1976.  9th ed.  Windholi, M., ed.  Merck
     and Co., Rahway, New Jersey
Isobutyl alcohol
Page 2
October 1985

-------
 NATIONAL  INSTITUTE FOR OCCUPATIONAL  SAFETY AND HEALTH  (NIOSH).
      1984.  Registry of Toxic Effects Of Chemical  Substances.
      Data lase.  Washington, D.C.  October 1984

 SAX,  N.I.   1975.  Dangerous Properties of Industrial Materials;
      4th  *d.  Van Nostrand Reinhold  Co., New York.  1,258 pages

 VERSCHUEREN, K.  1977•  Handbook of  Environmental  Data on Organic
      Chemicals.  Van Nostrand Reinhold Co., New York.  €59 pages

 WEAST, R.E., ed.  1981.  Handbook of Chemistry and Physics.
      62nd ed.  CRC Press, Cleveland, Ohio.  2,332  pages
Isobutyl alcohol
Page 3
October 198S

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                            ISOPROPYL  ETHER
        Although similar  to ethyl  ether,  isopropyl  ether  Is considered
   to be nort toxic and  irritating.  At high  concentrations it
   causes narcosis and death.

   CAS Number:   108-20-3
   Chemical  Formula:   (CHj) 2CHOCH(C13) 2
   I UP AC Name;   di-Isopropyl ether
   Important Synonyms  and Trade  Hanes:  2-Xsopropoxypropane,  IPE,
                                       DIPS,  di-isopropyloxide
   Chemical  and  Physical  Properties
   Molecular Height:   102.2
   Boiling Points   €5*C
   Melting Points   -fiO*C
   Specific  Gravity:   0.73 at  2Q»C
   Solubility in Mater:   2,000 fflg/ liter
   Solubility in Organics:   Miscible with alcohol and  ethyl ether
   Log Octanol/Water Partition Coefficient:   Approximately  2.5
                                             (calculated)
   Vapor Pressure:   130 ma ig  at 20*C
   Vapor Density:   3.52
   Plash Point:  -18*C (closed cup)

   Transport and Pate
        Mo specific information  on the transport and fate of  iso-
   propyl ether  was found in the sources  reviewed.  However,  likely
   transport and fate  mechanisms can be determined  froa information
   on  chemical and  physical properties and by inference from informa-
   tion on bis{2-chloroisopropyl)ether .
   Isopropyl ether
   Page  1
   October  19S5
                                                   ^TOsrrwm Associates
Preceding page blank

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     The relatively high vapor pressure of isopropyl alcohol
 indicates that  it probably volatilizes from surface water and
 soils.  It Is somewhat water soluble and therefore may leach
 through soil, although its log octanol/water partition coeffi-
 cient of approximately 2.S indicates that It Bay be adsorbed
 to soil organic*.  In one study, bis (2-chloroisopropyl) ether
 vas collected 150 miles downstream from a point source at the
 levels one would expect based on calculations using only river
 dilution factors.  This indicates that the ether is not volatilized
 degraded, or sorbed to any great degree.  The chemical is probably
 fairly persistent in the environment.  Conversion of the ether
 to a peroxide probably occurs in the environment, but the actual
 rate is unclear.
                                      *


 Health Effects

     No reports on earcinogenicity, mutagenicity, reproductive
 toxicity, or teratfegenicity were found in the literature reviewed.
 Isopropyl ether is considered to be somewhat more toxic and
 irritating than ethyl ether.  The only toxic effects exhibited
 were narcosis and death after the chemical was administered   ,
 at high concentrations (narcosis occurred at about 42,000 ag/ar) .
 The oral LD-0 in rats is 6,470 mg/kg.


 Toxicity to Wildlife and Domestic Aniaals

     Adequate data for characterization of toxicity of isopropyl
 ether to wildlife or domestic aniaals are not available.


 legul a t ions and Standards

 OSHA Standard (air) s  2,100 ag/a3 TWA

ACGIH Threshold Limit Values:  1,050 ag/a* TWA
                               1,320 mg/mj STEL


 REFERENCES

AMERICAN CONFERENCE 07 GOVERNMENTAL INDUSTRIAL HYGIENISTS (ACGIH) .
     1980.  Documentation of the Threshold Limit Values.  4th
     ed.  Cincinnati, Ohio.  488 pages

THE MERCK INDEX.  1976.  9th ed.  Windholi, M., ed.  Merck
     and Co., Rahway, Hew Jersey

NATIONAL IMSTITTJTS FOR OCCUPATIONAL SAFETY AND HEALTH  (NIOSH) .
     1984.  Registry of Toxic Effects of Chemical Substances.
     Data Base.  Washington, D.C.  July 1904


Isopropyl ether
Page 2
October 19SS
                                                                   J

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SAX, H.I.  1975.  Dangerous Properties of Industrial  Materials.
     4th «d.  Van Rostrand Reinhold Co.,  New York.  1,258  pages

U.S. ENVIRONMENTAL PROTECTION AGENCY (OSEPA).  1919,  Water-
     Related Environmental Fate of 129 Priority Pollutants.
     Washington, D.C.  December 1979.   EPA 440/4-79-029

VZRSCHUEREN, K.  1977.  Handbook of Environmental Data on  Organic
     Chemicals,  van Noatrand Reinhold Co.,  Mew York.  659 pages

WEAST, R.E., ed.  1981.  Handbook of Chemistry and  Physics,
     62nd ed.  CRC Press, Cleveland, Ohio.  2,332 pages
Itopropyl ether
Page 3
October 1985
                        3H1

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                                   LEAD
     Summary

          Lead Is a heavy octal that exists in one of three oxidation
     states, Of +2, and +4.   There Is suggestive evidence that some
     lead salts are carcinogenic,  inducing kidney tumors in mice
     and rats.  Lead is also a reproductive hazard, and it ean adversely
     affect the brain and central  nervous system by causing encephalo-
     pathy and peripheral neuropathy.  Chronic exposure to low levels
     of  lead can cause subtle learning disabilities in children.
     Exposure to lead ean also cause kidney damage and anemia, and
     it  nay have adverse effects on the innnune system.


     CAS Number:  7439-92-1

     Chemical Formula:  Pb

     IUPAC Name:  Lead


     Chemical and Physical Properties

     Atomic Weight:  207.19

     Boiling Point:  1,740»C

     Melting Point:  327.502»C

     Specific Gravity:  11.35 at 2Q«C

     Solubility in Water: Insoluble; some organic compounds are
                          soluble

     Solubility In Organics:   Soluble in HNO, and hot, concentrated
                              HI ***%          **
    Transport  and Fate

         Some  industrially  produced lead compounds are readily
    soluble  in water  (DSEPA 1979).   However,  metallic lead and
    the common lead minerals are  insoluble  in water.   Natural compounds
    of lead  art not usually mobile  in normal  surface  or groundwater
    because  the lead  leached from ores is adsorbed by ferric hydroxide
    or combines with  carbonate  or sulfate ions to form insoluble
    compounds.
    Lead
    Page  1
    October  19 S 5
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     Movement of  lead  and  its  inorganic and organolead corapourx
as participates in the atmosphere  is a aajor environmental
transport process.  Lead carried in the atmosphere can be reao\
by either wet or  dry deposition.  Although little evidence
is available concerning the photolysis of lead compounds in
natural waters, photolysis in  the atmosphere occurs readily.
These atmospheric processes are important in determining the
fora of lead entering aquatic  and  terrestrial systems.

     The transport of lead in  the aquatic environment is influ-
enced by the speciation of the ion.  Lead exists mainly as the
divalent cation in most unpolluted waters and becomes adsorbed
into particulate  phases.  However, in polluted waters organic
conplexation is most important.  Volatilization of lead compoun
probably is not important in most aquatic environments.

     Sorption processes appear to exert a dominant effect on
the distribution  of lead in the environment.  Adsorption to
inorganic solids, organic materials, and hydrous iron and man-
ganese oxides usually controls the mobility of lead and results
in a strong partitioning of lead to the bed sediments in aquatic
systems.  The sorption mechanism most important in a particular
system varies with geological  setting, pfl, Eh, availability
of ligandSf dissolved and particulate ion concentrations, salin-
ity,  and chemical composition.  The equilibrium solubility
of lead with carbonate, sulfate, and sulfide is low.  Over
most of the normal pH range, lead carbonate, and lead sulfate
control solubility of lead in  aerobic conditions, and lead
sulfide and the metal control  solubility in anaerobic conditions
Lead is strongly  complexed to  organic materials present in
aquatic systems and soil.  Lead In soil is not easily taken
up by plants, and therefore its availability to terrestrial
organisms is somewhat limited.

     Bioaccusiulation of lead has been demonstrated for a variety
of organisms, and bioconcentration factors are within the range
of 100-1,000.  Microcosm studies indicate that lead is not
biomagnified through the food  chain.  Biomethylation of lead
by microorganisms can remobilize lead to the environment.
The ultimate sink of lead is probably the deep oceans.


Health Effects

     There is evidence that several lead salts are carcinogenic
In ale* or rats,  causing tuaocs of the kidneys after either
oral or parenteral administration.  Data concerning the carcino-
gen icity of leai  in humans are inconclusive.  The available
data  are not sufficient to evaluate the carcinogenicity of
organic lead compounds or metallic lead.  There is equivocal
evidence that exposure to lead causes genotoxlcity in humans
and animals.  The available evidence indicates that lead presents
Lead
Page 2
October 19SS
                                                               -J

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a hazard to reproduction and exerts a toxie affect on conception,
pregnancy, and the fetus In humans and experimental animals
 (USEPA 1977,  1980).

     Many lead compounds are sufficiently soluble In body fluids
to be toxic {USEPA 1977, 19801.  Exposure of humans oc experi-
mental animals to lead can result in toxic effects in the brain
•nd central nervous system, the peripheral nervous system,
the kidneys,  and the hematopoietic system.  Chronic exposure
to inorganic  lead by ingestion or inhalation can cause lead
encephalopathy, and severe cases can result in permanent brain
damage.  Lead poisoning may cause peripheral neuropathy in
adults and children, and permanent learning disabilities that
are clinically undetec table in children may be caused by exposure
to relatively low levels.  Short-tern exposure to lead cm
cause reversible kidney damage, but prolonged exposure at high
concentrations may result in progressive kidney damage and
possibly kidney failure.  Anemia, due to inhibition of hemoblobin
synthesis and a reduction in the life span of circulating red
blood cells,  is an early Manifestation of lead poisoning.
Several studies with experimental animals suggest that lead
nay interfere with various aspects of the immune response.


Toxicity to Wildlife and Domestic Animals

     Freshwater vertebrates and invertebrates are more sensitive
to lead in soft water than in hard water (OSEPA 1980, 1983).
At a hardness of about 50 ag/liter CaCO,, the median effect
concentrations for nine families range iron 140 Mi/liter to
236,600 ug/liter.  Chronic values for Daphnia magna and the
rainbow trout are 12.26 and 83.08 ug/liter, respectively, at
a hardness of about 50 mg/liter.  Acute-chronic ratios calcu-
lated for three freshwater species ranged from 18 to 62.  Biocon-
centration factors, ranging from 42 for young brook trout to
1,700 for a snail, were reported,  freshwater algae show an
inhibition of growth at concentrations above 500 ug/liter.

     Acute values for twelve saltwater species range from 476 ug/
liter for the coaaon mussel to 27,000 ug/liter for the soft-
shell claa.  Chronic exposure to lead causes adverse effects
in mysid shrimp st 37 ug/liter, but not at 17 ug/liter.  The
acute-chronic ratio for this species is 118.  Reported biocon-
centration factors range from 17.5 for the Quahog clam to 2,570
for the blue missel.  Saltwater algae are adversely affected
at approximate lead concentrations mm low as 15.8 Mg/liter.

     Although lead is known to occur in the tissue of many
free-living wild animals, including birds, mammals, fishes,
and invertebrates, reports of poisoning usually, involve waterfowl,
There is evidence that lead, at concentrations occasionally
found near roadsides and smelters, can eliminate or reduce


Lead
fage 3
October 1985

-------
 populations  of  bacteria  and  fungi  on  leaf  turfacts  and  in  soil.
 Many  of  these microorganisms play  key roles  in  the  decomposer
 food  chain.

      Casts of lead  poisoning have  been reported for  a variety
 of  domestic  animals,  including  cattle,  horses,  dogs, and cats.
 Several  types of anthropogenic  sources are cittd as  the source
 of  lead  in these reports.  Because of their  curiosity and  their
 indiscriminate  eating  habits* cattle  experience th*  greatest
 incidence of lead toxicity among domestic  animals.


 Regulations  and Standards

 tab lent  Water Quality  Criteria  (OSEPJU i

      Aquatic Life (Proposed  Crittria)

      The concentrations  below are  for active lead, which is
      defined as the lead that passes  through a  0.45-um  membrane
      filter  after the  sample is acidified  to pH 4 with  nitric
      acid.

      Freshwater

          Acute toxicity:  e(1'34  tln(hardnesa)!  - 2.014)  w/llttt

          Chronic toxieity:  «U-34  tln(h«diWM)l - 5.245)

      Saltwater

          Acute toxicity:  220  ug/liter
          Chronic toxicity:   8.6 ug/liter

      Hunan Health

      Criterion:  50 ug/liter

 Primary  Drinking Water Standards   50  ug/liter

 NIOSH Recommended Standard:  0.10  mg/m TWA  (inorganic  lead)

OSHA  standard)  50  Mg/m3 TWA

ACGIH Threshold Limit. Values:
                       N
      0.1S ag/a| TWA (inorganic dusts  and fuaes)
      0.45 mg/m  STE1  (inorganic dusts and  fuaes)
Lead
Page 4
October 1985

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     Virtually no specific information on the toxicity of 2,4,5-T
to wildlife of dome*tic animals is available.  While 2,4,5-T
is thought to have relatively low toxicity for vertebrate species,
it has been reported that populations of invertebrates, including
beneficial insect species, have been adversely affected at
field concentrations.  Invertebrates nay be adversely affected
both directly because of the compound's toxicity and indirectly
because of the changes 2,4,5-T produces in vegetation growth
patterns.  Although 2,4,5-T is not reported to have large,
direct toxic effects on livestock, there are reports of animal
deaths due to alterations in plant chemistry and palatability
after 2,4,5-T treatment.

     Information on the effects of 2,4,5-T on aquatic species
is also limited.  Among fish, the LD-Q value for perch is
55 og/liter;  for guppies, 8 sag/liter? and for rainbow trout,
1.3 mg/liter.


Regulations and Standards

OSHA Standard (air):  10 mg/»3 TWA

ACGIH Threshold Limit Value;  10 mg/a3 TWA


REFERENCES

AMERICAN CONFERENCE OF GOVERNMENTAL INDUSTRIAL HYGIENISTS (ACGIH).
     1980.  Documentation of the Threshold Limit Values.  4th
     ed.  Cincinnati, Ohio.  488 pages

INTERNATIONAL AGENCY FOR RESEARCH ON CANCER (IARC).  1977.
     IARC Monographs on the Evaluation of the Carcinogenic
     Risk of Chemicals to Man.  Vol. 15:  Some Fuaigants, the
     Herbicides, 2,4-D and 2,4,5-T, Chlorinated Dibenzodioxins
     and Miscellaneous Industrial Chemicals.  World Health
     Organization, Lyon, France.  Pp. 273-299

THE MERCK INDEX.  1976.  9th ed.  Windholz, M., ed.  Merck
     and Co., Rahway, New Jersey

NATIONAL INSTITUTE FOR OCCUPATIONAL SAFETY AND HEALTH (NIOSH).
     1984.  Registry of Toxic Effects of Chemical Substances.
     Data Base.  Washington, D.C.  October 1984

NATIONAL RESEARCH COUNCIL OF CANADA.  1978.  Phenoxy Herbicides;
     Their Effects on Environmental Quality.  Subcommittee
     on Pesticides and Related Compounds, Ottawa, Canada.
     NRCC No. 16075.  440 pages
2,4,5-Trichlorophenoxyacetic acid
Page 3
October 1985
                                                   Qerwit Aaaoeiaca*

-------
SAX, H.I.  1975*  Dangerous Properties of Industrial Materials.
     4th *d.  Van Hostrand Reinhold.Co,, New York*  1,258 pages

VERSCBUEFUEM, K.  1977.  Handbook of Environmental Data on Organi
     Chtaiicall.  Van Hostrand Reinhold Co., He* fork.  659 pages

VETERAHS ADMINISTRATION (VA).  1982.  Review of Literature
     on Herbicides, Including fhenoxy H«rbicid«s and A»»ociated
     Sioiins.  Vols. I and 2:  Analysis of Littrtturt and Bibli-
     ography.  D«pact»«nt of Medicine and Surgery, Washington, o

VETERANS ADMINISTRATION (VA).  1984.  Review of Literature
     on Herbicides, Including Phenoxy Herbicides and Associated
     Dioxins.  Vols. 3 and 4.  Analysis and Bibliography of Re-
     cent Literature on Health Effects.  Department of Medicine
     and Surgery, Washington, D.C.
2,4,5-Trichlorophenoxyacetic acid
Page 4
October 1985

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REFERENCES

AMERICAN CONFERENCE OF GOVERNMENTAL INDUSTRIAL HYGIENISTS  (ACGIH),
      1980.  Documentation of the Threshold Limit Values.   4th ed.
      Cincinnatit Ohio.  481 pages

DOULL, J., KLAASSSN, L.D., and AHDUR, M.O., eds.  1980.  Casarett
      and Doull's Toxicology:  The Basic Science of Poisons.
      2nd ed.  Macnillan Publishing Co., New York.  778 pages

INTERNATIONAL AGENCY FOR RESEARCH ON CANCER CIARC) .  1980 .
      IARC Monographs on the Evaluation of Carcinogenic Risk
      of Chemicals to Humans.  Vol. 23:  Some Metals and Metallic
      Compounds.  Woeld Health Organization! Lyon, Prance.
      Pp. 325-415

NATIONAL INSTITUTE FOR OCCUPATIONAL SAFETY AND HEALTH (NXOSB).
      1983.  Registry of Toxic Effects of Chemical Substances.
      Data Base.  Washington, D.C.  October 1983

NRIAGO, J.O., ed.  1978.  The Siogeochemistry of Lead in the
      Environment:  Part B.  Biological Effects.  Elsevier/North^
     Holland Bioaedical Press, New York.  397 pages

U.S.  ENVIRONMENTAL PROTECTION AGENCY (OSEPA).  1977.  Air Quality
     Criteria for Lead.  Office of Research and Development,
     Washington, D.C,  December 1977.  EPA 600/8-77-017

U.S.  ENVIRONMENTAL PROTECTION AGENCY (USEPA).  1979.  Water-
      Related Environmental Fate of 129 Priority Pollutants.
     Washington, D.C.  December 1979.  EPA 440/4*79*029

U.S. ENVIRONMENTAL PROTECTION AGENCY {OSEPA).  1980.  Ambient
     Water Quality Criteria for Lead.  Office of Water Regula-
      tions and Standards, Criteria and Standards Division,
     Washington, D.C.  October 1980.  EPA 440/5-80-057

O.S. ENVIRONMENTAL PROTECTION AGENCY (OSEPA).  1983.  Draft
     Revised Section B of Ambient Water Quality Criteria for
     Lead.  Office of Water Regulations and Standards, Criteria
      and Standards Division, Washington, D.C.  August 1983

O.S. ENVIRONMENTAL PROTECTION AGENCY (OSEPA).  1984.  Health.
     Effects Assessment for Lead.  Final Draft.  Environmental
     Criteria and Assessment Office, Cincinnati, Ohio.  September
      1984.  ICAO-CIN-HQ55

WEAST, R.E., ed.  1981.  Handbook of Chemistry and Physics.
     62nd ed.  CRC Press, Cleveland, Ohio.  2,332 pages

WORLD HEALTH ORGANIZATION.  1977.  Environmental Health Criteria:
      3.  Lead.  World Health Organization, Geneva.  1(0 pages


Lead
Page  S
October 1985

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                              LITHIUM


 Summary

       Lithium  produced  cleft  palate  in  the  offspring  of  pregnant
 eats  and  mice,  and  it  caused other  malformations  in  the rat
 fetuses.  Exposure  to  various  lithium  compounds can  cause  eye,
 skin,  and mucous membrane  irritation;  pulmonary emphysema;
 nausea- blurred vision;  coma;  and epileptic  seizures.


 Background Information

       Lithium  is a soft white metal  that  reacts exotherraally
 with  nitrogen at room  temperature when the humidity  is  moderately
 high.  It burns and explodes in  contact  with water,  nitrogen,
 acids, and oxidizing agents.

 CAS Numbers   7439-93-2

 Chemical  Formula:   Li

 IUPAC  Name:   Lithium

 important Synonyms  and Trade Names:  Lithium metal


 Chemical  and  Physical  Properties

 Molecular Height:   €.9

 Boiling Points  1342*C

 Melting Points  180.5*C

 Specific  Gravity:   0.534 at  20°C

 Solubility in Water:   Decomposes in cold water

 Solubility in Organics:  Insoluble

 Vapor  Pressure:  1  mm  Hg at  723*C

 Plash  Point:  Not pertinent  (combustible solid)
                          v

 Transport and Pate

      No specific information on  the transport and fate  of  lithium
 was found in  the literature  reviewed.  Lithium metal decomposes
 in water  and  forma  soluble lithium  salts.  It moves  readily


 Lithium
 Page  1
 October 1985


Preceding page blank
                          iCQ

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with ground and surface water.  The movement of lithium through
soil is limited by the cation exchange potential of the soil.


Health Effects

     Th«r« were no data on carcinogenic or mutagenic effects
in the literature reviewed.

     Rats wees dosed intraperitonally with 50 mg/day on days
lr 4, 7, and 9 of gestation, followed by doses of 20 mg daily
until day 17,  Malformations were seen in the eye (62%) and
external ear (451); cleft palate also occurred (39%) (Wright
et al. 1970).  Cleft palate was also observed in sice  (Szabo 1970

  ,  The lethality of lithium chloride is dependent upon the
lia  level in the body.  Dogs survived an oral dose of  50 mg/kg
for 150 days when they had normal Ha  levels but died  within
8 to 12 days if they had a low Na  level.  The oral LD.. for
lithiua chloride in rats was determined to be 757 ng/kg.  The
LDSO in dogs for Li.CO. was measured as 500 ag/kg.  Lithium
compounds cause nausea? vomiting; skin, eye, and lung  irritation;
and pulmonary emphysema in huaans at doses as low as 7 ag/kg.

     The chronic health effects of lithiua are anorexia, fatigue,
dehydration, diarrhea, vomiting, blurred vision, coaa, and
epileptic seizures.  The target organ is the kidney, although
lithium is distributed fairly evenly throughout the body.


Toxieity to Wildlife and Domestic Animals

     There were no data available on the toxicity of lithium
to wildlife and domestic animals.


Regulati ona and 31andards

ACGIH Threshold Limit Value:  0.025 mg/a3 TWA (lithium hydride)


REFERENCES

AMERICAN CONFERENCE OP GOVERNMENTAL INDUSTRIAL HYGIENISTS {ACGIH)
     1980.  Documentation of the Threshold Limit Values*.  4th
     ed.  Cincinnati, Ohio.  488 pages

HATIOHAL IHSTITtJTB FOR OCCUPATIOHAL SAFETY AMD 1EALTI  (MIQSH).
     1984.  Registry of Toxic Effects of Chemical Substances.
     Data Base.  Washington, B.C.  July 1984

SZABO, 1.9.  Teratogenic effect of lithiua carbonate in the
     foetal mouse.  1970.  Mature 225i73

Lithiua
Page 2
October 1985

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VERSCHUEREN, K.  1977.  landboofc of Envitoruaental Data on Organic
     Chtmicali.  Van Nostrand Reinhold Co., New York.  €59 pages

WEAST, R.E., ed.  1981.  Handbook of Chemistry and Physics.
     62nd ed.  CRG Press, Cleveland, Ohio.  2,332 pages

WHISHT, T.L., HOFFMAN, L.H., and DAVIES, J.  1970.  Lithium
     teratogenicity.  Lancet 2:876
Lithium
fag* 3
October 1985
                                                  [Qvrwne Aasoeia

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                            MAGNESIUM


Summary

     Exposure to magnesium oxide fumes can cause metal fume
fever  in humans.  Exposure to magnesium oxide dust can irritate
the eyes and respiratory tract.  Ingestion of very high levels
of magnesium salts can cause central nervous sytem effects;
it can also have a laxative action.


Background I reformation

     Magnesium is the eighth most abundant element on earth.
It is very reactive chemically and do.es not occur uncombined
in nature.  Finely divided magnesium can react with water  to
yield hydrogen gas and magnesium hydroxide.  However, reaction
of solid magnesium with water is self*limiting because of  the
formation of a film of magnesium hydroxide.  As a result,  ele-
mental magnesium is considered insoluble in water.

CAS Humber:  7439-95-4

Chemical Formula:  Mg

IUPAC name:  Magnesium


Chemical and Physical Properties     -  *

Atomic Height:  24.312

Boiling Point;  1107»C

Melting Point:  648.8»C

Specific Gravity?  1.738

Solubility in Water:  Insoluble; most salts art very soluble


Transport and Fate

     Most magnesium salts are very soluble at pH levels normally
found in natural waters, and the magnesium ion is readily  trans-
ported in surface water/soil, and groundwater.  The extent of
magnesium transport in soil is dependent! in part, on the  cation
exchange capacity of the soil.  Evaporation of ocean spray
particles and subsequent atmospheric transport of magnesium
Magnesium
Page 1
October 1985
Prec
   eding page b^

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can occur.  Atmospheric  transport of dusts and fumes  of  compounds
•uch as magnesia oxide can also occur.


Health Effects

     There  is no evidence to suggest that magnesium has  carcino-
genic, autagenic, teratogenic, or reproductive effects in humans
or experimental animals.  Magnesium oxide fumes can produce
•etal fume  fever in humans and experimental animals.  Exposure
to magnesium oxide dust  may cause irritation of the eyes and
respiratory tract.  Human exposure to magnesium usually occurs
by ingestion.  Magnesium is an essential element for  humans,
animals, and plants.  Ingestion of 3.1 to 4.2 mg/kg/day  is
thought to  be adequate for maintenance of magnesium balance
in humans.  The average  adult American is estimated to ingest
240 to 480 mg/kg/day  in  food and water.  However, magnesium
is absorbed relatively poorly by the gastrointestinal tract
and also is readily excreted in the urine.  Excessive magnesium
retention in the body generally only occurs as a result of
severe kidney disease.   Symptoms of hypermagnesemia can  include
a sharp drop in blood pressure, and respiratory paralysis due
to central nervous system depression.  Ingestion of magnesium
salts at concentrations  over 700 mg/liter can have a  laxative
effect.  However, humans can adapt to ingestion of these levels
in a relatively short time.  Magnesium has a vary unpleasant
taste in water at concentrations producing toxic effects.

     Different magnesium compounds vary in the severity of
their toxic effects to experimental animals.  Such effects
include central nervous  system and purgative effects  similar
to those seen in humans.  Subcutaneous injection of powdered
magnesium or magnesium alloys can produce symptoms in experi-
mental animals resembling gas gangrene.  Application of powdered
magnesium to abraded skin can produce an inflammatory reaction.
However, these types of  skin effects have not been reported
in exposed workers.


Toxicitv to Wildlife and Domestic Animals

     Available data are  not adequate to characterize the toxicity
of magnesium to wildlife or domestic aniaals.  Observed effects
are generally related to deficiency symptoms.


Regulations and Standards

OS1A Standard;  15 «g/m3 {magnesium oxide fume)

ACGIH Threshold Limit values:
Magnesium
fage 2
October 1985

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     10 Bg/B    **  (Bagnesite, nuisance participate)
     20 ag/ar STEL  (aagnesite, nuisance particulate)

U.S. Department of Transportation:  Flammable solid; dangerous
                                    when wet
REFERENCES

AMERICAN CONFERENCE OP GOVERNMENTAL INDUSTRIAL EYGIENISTS (ACGIH),
     1980.  Documentation of the Threshold Limit Values.  4th
     ed.  Cincinnati, Ohio.  488 pages

CLAYTON, G.D., and CLAYTON, F.E., eds.  1181.  fatty's Industrial
     Hygiene and Toxicology.  Vol. 2A:  Toxicology.  3rd rev. ed.
     John Wiley and Sons, New York.  2,878 pages

DOULL, J., KLAASSEN, C.D,, and AMDTO, M.O., eds,  1980.  Casarett
     and Doull's Toxicology:  The Basic Science of Foisons.
     2nd ed.  Macaillan Publishing Co., Mew York.  778 pages

NATIONAL ACADEMY OP SCIENCES (MAS).  1977.  Drinking Hater and
     Health.  Safe Drinking Water Committee, Washington, D.C.
     939 pages

NATIONAL INSTITUTE FOR OCCUPATIONAL SAFETY AND HEALTH (NIOSH) .
     1984.  Registry of Toxic Effects of Chemical Substances.
     Data Base.  Washington, D.C.  April 1984

WEAST, R.E., ed;  1981.  Handbook of Chemistry and Physics.
     6.2nd ed.  CRC Press, Cleveland, Ohio.  2332 pages
Magnesium
fage 3
October 1985

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                               MANGANESE
   Summary
        Manganese chloride produced lymphomas and manganese sulfate,
   tumors after Injestion into mice.  In humans,  chronic exposure
   to manganese causes degenerative changes  in the central nervous
   system in the form of a Parkinson-like disease; liver changes
   also occur.   Acute exposure causes manganese pneumonitis.


   CAS Number:   7439-96-5

   Chemical Formula:   Mn

   TUPAC Name:   Manganese


   Chemical and Physical Properties

   Atomic Weight:  54.938

   Boiling Points  1962«C

   Melting Points  1244»C

   Specific Gravity:   7.20

   Solubility in Water:  Decomposesj some compounds are soluble


   Transport and Pate

        Manganese occurs most commonly in the +2  and +4 oxidation
   states in aquatic  systems.  Its solubility depends to a great
   extent on pH, dissolved oxygen, and presence of complexing
   agents.  In  saltwater, it is estimated that 85% or more of the
   manganese present  exists in a soluble form.  In freshwater,
   manganese can occur as the soluble ion, in complex organic ions,
   or in colloidal suspensions.  Manganese often  occurs at higher
   concentrations near the bottom of stratified lakes because it
   can be released from sediments, as the manganous ion, under
   reducing conditions.

        In the  soil,  the concentration and chemical form in which
   manganese occur can be affected by pH, cation  exchange capacity,
   drainage, organic  matter content, and other factors.  The solu-
   bility of manganese is increased at low pH and under reducing
   conditions.   The presence of high concentrations of chlorides,
   nitrates, or sulfates may also increase solubility.  Under
   these conditions,  manganese is more easily taken up by plants


   Manganese
   Page 1
   October 1985

                                                  Qcismsne Associates

Preceding page blank

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 or  transported  in  aqueous  solution.  Lack of  sufficient cation
 exchange  sites, which are  provided by organic matter or clay,
 can also  result in greater leaching of manganese to surface or
 groundwater.

     Ataospheric transport of manganese fames or dusts can
 occur.  These materials can be returned to the earth by wet
 or  dry deposition.


 Health Effects

     There are no  epidemiological studies suggesting that man-
 ganese or its compounds are carcinogenic or have teratogenic or
 reproductive effects in humans.  Exposure to manganese chloride
 by  intraperitoneal or subcutaneous routes was reported to cause
 lynphonas in nice.  Manganese sulfate was found to produce
 tumors after intraperitoneal administration in sice.  Ho other
 reports of unequivocal carcinogenic activity are available for
 common manganese compounds.  Some manganese compounds, notably
 manganese chloride, have exhibited mutagenic activity in a
 variety of test systems.  Manganese compounds do not appear
 to  be teratogenic, however.

     In humans, manganese dusts and compounds have relatively
 low oral and dermal toxicity, but they can cause a variety
 of  toxic effects after inhalation exposure.  Acute exposure
 to  very high concentrations can cause manganese pneuaonitis,
 increased susceptibility to respiratory disease, and pathologic
 changes including epithelial necrosis and aononuclear prolifera-
 tion.  Chronic manganese poisoning Is sore common, but generally
 occurs only among  persons occupationally exposed to manganese
 compounds.  Degenerative changes in the central nervous system
 are the major toxic effects.  Early symptoms Include emotional
 changes, followed  by a aasklike face, retropulsion or propulsion,
 and a Parkinson's-like syndrome, , Liver change* are also frequently
 seen.  Individuals with an iron deficiency may be more suscept-
 ible to chronic poisoning.

     Duplication of human exposure symptoms in experimental
 animals has only been partially successful.  In rabbits exposed
 by  inhalation to manganese dust* manganese pneuaonitis did
 not develop, but fibrotic changes in the lungs were observed.
Central nervous system effects characteristic of chronic expo-
 sure in nuaans have only been reproduced in monkeys.
                       •»

Toxicity to Wildlife and Domestic Animals

     Adequate data for characteriiation of the toxicity of
manganese to wildlife or doaestic aniaals are not available.
Manganese
Page 2
October 1985

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 repotted  tot  emoryos  of  trie  oyster  Crassostrta  virginica.
 for  the softshell  elan Mya arenaria a  166-hour  LC-.I  galue  of
 300  ag/liter  ii  reported.                         50


 Regulation* and  Standards

 OSHA standard:   5  ag/m3  Ceiling Level

 ACGIH Threshold  Limit Values:

      1 tog/mi*  TWA (fume)
      3 ng/mf  STEL  (fume)
      5 mg/m   Ceiling  Level  (dust  and compounds)


 REFERENCES

 AMERICAN  CONFERENCE Of GOVERNMENTAL INDUSTRIAL  HYSISNISTS  (ACGIH},
      1980.  Documentation of the  Threshold Limit values.   4th
      ed.  Cincinnati, Ohio.  488  pages

 DOULL, J,, KLAASSEN,  C.D., and AMOUR, M.O., eda.  1S80.  Casarett
      and  Doull's Toxicology:  The Basic Science of Poisons.
      2nd  ed.  Hacmillan  Publishing  Co., Hew'fork*  778 pages

 EISLER, R.  1977.  Acute tozicities of selected heavy metals
      to the softshell clam, Mya arenaria.  Bull. Environ.
      Contarn.  Toiicol. 17s137^111

 NATIONAL  ACADEMY OF SCIENCE  (MAS).  1973.  Medical and Biolo-
      gical Effects of Environmental Pollutants!  Manganese.
      Washington, D.C.  191 pages

 NATIONAL  ACADEMY OF SCIENCES (HAS).  1977.  Drinking Water
      and  Health.   Safe Drinking Water Committee, Washington,
      D.C.  939 pages

 NATIONAL  INSTITUTE FOR OCCUPATIONAL SAFETY AND  HEALTH (MIOSH).
      1983.  Registry  of  Toxic Effects of Chemical Substances.
      Data Base.  Washington, D.C.   October 1983

 U.S.  ENVIRONMENTAL PROTECTION AGENCY (USEfA).   1984.  Health
      Effects  Assessment  for Manganese.  Environmental Criteria
      and  Assessment Office, Cincinnati, Obio.   September 1984.
      ECAO-CIH-H057  (Final Draft)

WEAST, R.E.,  ed.   1981.  Handbook of Chemistry  and Physics.
      62nd ed.  CRC Press, Cleveland, Ohio.  2332 pages
Manganese
Page 3
October 198S

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                             MERCURY
Summary
     Both organic and inorganic forms of mercury are reported
to be teratogenic and embryotoxic In experimental animals.
In humans, prenatal exposure to raethylmercury has been associated
with brain damage.  Other major target organs for organic mercury
compounds in humans are the central and peripheral nervous
system and the kidney.  In animals, toxic effects also occur
in the. liver, heart, gonads, pancreas, and gastrointestinal
tract*.'  Inorganic mercury is generally less acutely toxic than
organic mercury compounds, but it does affect the central nervous
system adversely.
Background Information

     Several forms of mercury, including Insoluble elemental
mercury, inorganic species, and organic species, can exist
in the environment.  In general, the mereurous  (+1) salts are
much less soluble than the more commonly found mercuric (+2)
salts.  Mercury also forms many stable organic complexes that
are generally much more soluble in organic liquids than in
water.  The nature and solubility of the chemical species that
occur in an environmental system depend on the redox potential
and the pa of the environment.

CAS Number*  7439-97-6

Chemical Formula:  Hg

IUPAC Name:  Mercury


Chemical and Physical Properties (Metal)

Atomic Weight:  200.59

Boiling Point:  35S.58*C

Melting Points  -38.87*C

Specific Gravity:  13.5939 at 2Q*C

Solubility in Water*  81.3^ug/liter at 30«Cf some salts and
                      organic compounds are soluble
Mercury
Page 1
October 1985
                                                              iacaa
   Preceding page blank

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 Solubility in  Organic*;   Depends  on  chemical  species

-Vapor  Pressures   0.0012  mm Bg  at  20*C


 Transport  and  Fate

     Mercury and  certain of  its compounds,  including several
 inorganic  species and dimethyl mercury, can volatilize to the
 atmosphere iron aquatic  and  terrestrial sources,  volatilization
 is  reduced by  conversion of  metallic mercury  to completed species
 and  by-deposition of HfS in  reducing sediments, but even so
 atmospheric transport is the major environmental distribution
 pathway  for mercury.  Precipitation  is the  primary mechanism
 for  removal of mercury from  the atmosphere.   Photolysis is
 important  in the  breakdown of  airborne mercurials and may be
 important  in some aquatic systems.   Adsorption onto suspended
 and  bed  sediments is probably  the most important process determin-
 ing  the  fate of mercury  in the aquatic environment.  Sorption
 is  strongest into organic materials.  Mercury in soils' is gener-
 ally complexed to organic compounds.

     Virtually any mercury compound  can be  remobilized in aquatic
 systems  by aicrobial conversion to methyl and dimethyl forms.
 Conditions reported to enhance biomethylation include large
 amounts  of available mercury,  large  numbers of bacteria, the
 absence  of strong complexing agents, near neutral pH, high
 temperatures, and moderately aerobic environments.  Mercury
 is  strongly bi©accumulated by  numerous mechanisms.  Methylmercury
 is  the most readily accumulated and  retained  fora of mercury
 in  aquatic biota, and once it  enters a biological system it
 is very  difficult to eliminate.


 Health Effects

     When  administered by intraperitoneal injection, metallic
 mercury  produces  implantation  site sarcomas in rats.  No other
 studies  were found connecting  mercury exposure iritis carcinogenic
 effects  in  animals or humans.  Several mercury compounds exhibit
 a variety  of genotoiie effects in eukarvotes.  In general,
 organic  mercury compounds are  more toxic than inorganic compounds.
Although brain damage due to prenatal exposure to methylmercury
 has occurred in human populations, no conclusive evidence is
 available  to suggest that mercury causes anatomical defects
 in humans.  Embryotoxicity ,and teratogenicity of methylmercury
 has been reported for a  variety of experimental animals.  Mer-
curic chloride is reported to  be  teratogenic  in experimental
animals.  No conclusive  results concerning  the teratogenic
effects  of  mercury vapor  are available.
Mercury
Page 2
October 19SS

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     In humans, alkyl mercury compounds pass through the blood
brain barrier and the placenta very rapidly, in contrast to
inorganic mercury compounds.  Major target organs are the central
and peripheral nervous systems, and the kidney.  Methylmercury
is particularly hazardous because of the difficulty of elimi-
nating it from the body.  In experimental animals, organic
•trcury compounds can produce toxic effects in the gastrointes-
tinal tract, pancreas, liver, heart, and gonads, with involvement
of the endocrine, imrounocompetent, and central nervous systems.

     Elemental mercury is not highly toxic as an acute poison.
However, inhalation of high concentrations of mercury vapor
can cause pneuraonitis, bronchitis, chest pains, dyspnea, cough-
ing, stomatitis, gingivitis, salivation, and diarrhea.  Soluble
mercuric salts are highly poisonous on ingestion, with oral
LD.Q values of 20 to 60 mg/kg reported.  Mercurous compounds
are less toxic when administered orally.  Acute exposure to
mercury compounds at high concentrations causes a variety of
gastrointestinal symptoms and severe anuria with uremia.  Signs
and symptoms associated with chronic exposure involve the central
nervous system and include behavioral and neurological distur-
bances.


Toxicity to Wildlife and Domestic Animals

     The toxicity of mercury compounds has been tested in a
wide variety of aquatic organisms.  Although methylmercury
appears to be more toxic than inorganic mercuric salts, few
acute or chronic toxicity tests have been conducted with it.
Among freshwater species, the 96-hour LC-. values for inorganic
mercuric salts range from 0.02 ug/lit«r for crayfish to 2,000 ug/
liter for caddisfly larvae.  Acute values for methylmeccuric
compounds and other mercury compounds are only available for
fishes.  In rainbow trout, methylmercurie chloride is about
ten times more toxic to rainbow trout than mercuric chloride,
which is acutely toxic at about 300 ug/liter at 10*C.  Methyl-
mercury is the most chronically toxic of the tested compounds,
with chronic values for Daphnia magna and brook trout of 1.00
and 0.52 Mg/liter, respectively.The acute-chronic ratio for
Daphnia magna is 3.2.

     Mean acute values for saltwater species range from 3.5
to 1,680 pg/liter.  In general, molluscs and crustaceans are
more sensitive than fish to the acute toxic effects of mercury.
A life-cycle experiment with the mysid shrimp showed that inor-
ganic mercury at a concentration of l.C ug/liter significantly
influences time of appearance of first brood, time of first
spawn, and productivity.  The acute-chronic ratio for the aysid
shrimp is 2.9.
Mercury
Page 3
October 1985

                                                ^Jcsem«nt Ammoc

-------
      Chronic dietary exposure of  chickens  to  mercuric  chloride
 at growth  inhibitory levels  causes  immune  suppression,  with
 a  differential  reduction effect on  specific iaununoglobulins.
 Regulations  and Standards
 Ambient Water Quality Criteria (DSEPA):
      Aquatic Life  (Proposed  Criteria)
      Freshwater
          Acute toxicity:    1.1 ug/liter
          Chronic  toxicity;    0,20  ug/liter
      Saltwater
          Acute toxicity:    1.9 ug/liter
          Chronic  toxicity:    0.10  ug/liter

    '  Hunan Health
      Criterion;  144  ng/liter
 Primary Drinking Water Standard:  0.002 ng/liter
 NZOSH Recommended  Standard;   0.05 mg/m3 TWA (inorganic  mercury)
 OSHA  Standard!   0.1 mg/n3 Ceiling Level
 ACGIH Threshold Limit Values:
      0.01 ag/a| TWA  (alkyl compounds)
      0.03 ag/af STEL  (allcyl  compounds)
      0.05 mg/m* TWA  (vapor)
      0.1 mg/m TWA (aryl  and  inorganic compounds)

 REFERENCES
AMERICAN CONFERENCE OF GOVERNMENTAL INDUSTRIAL HYGIENISTS  (ACGIH).
      1980.  Documentation of  the Threshold Limit values.  4th
      ed.  Cincinnati, Ohio.   4S8 pages
BRIDGER, M.A., and THAXTQJf, J.P.  1983.  Humoral immunity in
      the chicken as affected  by mercury.  Arch. Environ. Contam.
     Toxicol. 12145-49
Mercury
Page 4
October 1985

-------
NATIONAL INSTITUTE FOR OCCUPATIONAL SAFETY AND HEALTH (NIOSH).
     1983.  Registry of Toxic Effects of Chemical Substances
     Data Base.  Washington, D.C*  October 1983

SHEFARD, T.H.  1980.  Catalog of Teratogenic Agents.  3rd ed.
     Johns Hopkins University Press, Baltimore.  410 pages

O.S. ENVIRONMENTAL PROTECTION AGENCY (USEPA).  197t.  Water-
     Related Environmental Fate of 129 Priority Pollutants.
     Washington, D.C.  December 1979.  EPA 440/4-79-029

U.S. ENVIRONMENTAL PROTECTION AGENCY (USEPA).  1980.  Ambient
     Water Quality Criteria for Mercury.  Office of Water Regu-
     lations and Standards, Criteria and Standards Division,
     Washington, D.C.  October 1980.  EPA 440/5-80-058

U.S. ENVIRONMENTAL PROTECTION AGENCY (USEPA).  1984.  Water
     quality criteria; Request for comments.  Fed. Reg.  49:
     4551-4553

U.S. ENVIRONMENTAL PROTECTION AGENCY (USEPA).  1984.  Health
     Effects Assessment for Mercury.  Environmental Criteria
     and Assessment Office, Cincinnati, Ohio.   September 1984.
     ECAO-CXN-H042  (Final Draft)

WEAST, R.E., ed.  1981.  Handbook of Chemistry and Physics.
     62nd ed.  CRC Press, Cleveland, Ohio.  2,332 pages

WORLD HEALTH ORGANIZATION  (WHO).  1976.  Environmental Health
     Criteria:  1,  Mercury.  World Health Organization, Geneva.
     131 pages
Mercury
Page I
October 1985
                                                 [Ctomant

-------

-------
                         METHAC1YLIC ACID
                  MITIACRYLIC ACID, METHYL ESTER
 Summary
      Methacrylic acid caused DNA damage In E3cherichia colI,
 and methyl methacrylate was found to be rautagenic  using the
 Ames assay.  Methyl nethacrylate caused fetal  deaths  and develop-
 mental abnormalities in rats.   Exposure to methacrylic acid
 in the air can cause eye irritation in humans.


 CAS Number:  Methacrylic acid;   79-41-4
              Methacrylic acid,  aethyl ester:   80-62-6

 Chemical Formula:  Methacrylic  acid:  C2H2CH3CQQI
                    Methacrylic  acid, methyl isther:   C2H2CH3COOCH3

 IUPAC Name:  Methacrylic acid:   2-Methyl-2-propenoate
              Methacrylic acid,  methyl esther:   Methyl-2-methyl-
                2-propenoate

 Important Synonyms and Trade Names:

      Methacrylic acid:  Methacrylate
      Methacrylic acid, aethyl esther:  Methyl  methacrylate,  Pegalan


 Chemical and Physical Properties

 Molecular weight:  Methacrylic  acid:  86
                    Methacrylic  acid, methyl esther:   100

 Boiling Point:  Methacrylic acid:  1I3*C
                 Methacrylic acid, aethyl esther:   100*C

 Melting Point:  Methacrylic acid:  1€*C
                 Methacrylic acid, aethyl esther:   -48»C

 Specific Gravityi  Methacrylic  acid:  1.015 at 20*C
                    Methacrylic  acid, methyl esther:   0.994 at 20*C

 Solubility in Wateri  Slightly  soluble in water

 Solubility in Organics:  Misciblc in alcohol,  ether,  and acetone

 Log OctaneI/Water Partition Coefficient:

      Methacrylic acidt  0.65 (calculated}
      Methacrylic acid, methyl esthert  1.15 (calculated)
 Methacrylic acid
 Page 1
 October  19S5
Preceding page blank

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Vapor Pressures  Methacrylie acids  0.65 an Bg at 2Q*C
                 Methacrylic acid, methyl esther:  40 ag/Hg at 25°

Vapor Density:  Methacrylie acid;  297

Plash Pointi   77*C


Transport and  Fate

     The limited information available on the transport and
fate of methacrylic acid  (methacrylate) and methacrylic acid,
methyl esther  (methyl methacrylate) suggests that microbial
biodegradation is an important fate process for both compounds.
Methyl methacrylate is probably somewhat volatile and may also
be hydrolyzed  in a slightly acidic aqueous solution to methacrylate
and aethanol.


Health Effects

     No data on the carcinogenic, embryotoxie, or teratogenic
properties of  methacrylic acid were found in the literature
reviewed.  It  did cause DtfA damage in Eseherichia eoli.  Direct
eye or skin contact with aethacrylic acid can result in blindness
or corrosion of the akin, but exposure to a saturated atmosphere
of 3,500 mg/m  for 7 hours caused only eye irritation in rats.
Rats exposed via inhalation to 1,050 mg/m  for 6 hours a day
for 20 days suffered slight renal congestion.  The dermal I*D.Q
for rabbits is 500 to 1,000 mg/kg.

     Methyl methacrylate was administered to male and female
wistar rats in their drinking water for two years, and no treat-
ment-related tumors were observed*  Nor were any tumors found
after rats had methyl methacrylate applied to the back of their
necks 3 times  per week for 4 months; the rats were kept for
the rest of their lives.  Solid pieces of methyl methacrylate
have caused sarcomas at the sites of implantation.  Thus, the
evidence on the carcinogenicity of methyl methacrylate is incon-
clusive.  Methyl methacrylate was found to be mutagenic using
the Ames assay without activation and to be elastogenic in
rat bone Barrow cells after inhalation exposure of 4 mg/a
for IS weeks.  There is evidence that inhalation exposure to
sufficiently high levels of methyl aethaerylate can cause fetal
deaths and developmental abnormalities in rats.  The rat oral
LD50 is 7.87 f/Jtfj for the mouse, it is 5.2 g/kg.


Toxieity to Wildlife and Domestic Animals

     Although  no information was available in the literature
reviewed on the environmental toxicity of methacrylic acid,


Methacrylie acid
Page 2
October 1985


-------
Halted information is available foe methyl methacrylate.
The TL- (24-96 hour) values for the bluegill, fathead minnow,
and gufpy range from 159 to 500 »g/liter.  The threshold for
inhibition of all multiplication of the bacterium Pseudqmojjas
putida is 100 mg/literj cell mutiplication of the alga Microsystie
aetuginous is inhibited at 120 ing/liter.


Regulations and Standards

OSHA Standard (air):

     Methacrylic acid, methyl esthers  410 ng/«3 TWA

ACGIH Threshold Limit Values *

     Methacrylic acid:  70 »g/m3 TWA           ,
     Methacrylic acid, methyl esther:  410 mg/m^ TWA
                                       510 mg/m3 STEL

REFERENCES

AMERICAN CONFERENCE OF GOVERNMENTAL INDUSTRIAL HYGIENISTS  (ACGIH).
     1980.  Documentation of the Threshold Limit values.   4th
     ed.  Cincinnati, Ohio.  488 pages

INTERNATIONAL AGENCY FOR RESEARCH ON CANCER  (IARC).  1979.
     IARC Monographs on the Evaluation of the Carcinogenic
     Risk of Chemicals to Humans,  vol. 19:  Some Monomers,
     Plastics and Synthetic Elastomers, and Acrolein.  World
     Health Organization, Lyon, France.  9. 187

LYMAN, W.J., REEHL, W.F., and ROSENBLATT, D.H.  1982.  Handbook
     of Chemical Property Estimation Methods:  Environmental
     Behavior of Organic Compounds.  McGraw-Hill Book Co.,
     New York

THE MERCK INDEX.  1976.  9th ed.  Windholz, M., ed.  Merck
     and Co.f Rahway, New Jersey

NATIONAL INSTITUTE FOR OCCUPATIONAL SAFETY AND HEALTH (NIOSH).
     1984.  Registry of Toxic Effects of Chemical Substances.
     Data Base.  Washington, D.C.  October 1984

SAX, N.I.  1975.  Dangerous Properties of Industrial Materials.
     4th ed.  Van Hostrand Reinhold Co., New York.  1,258  pages

U.S. ENVIRONMENTAL PROTECTION AGENCY (USEPA).  1979.  Water-
     Related Environmental Fate of 129 Priority Pollutants.
     Washington, D.C.  December 1979.  EPA 440/4-79-029
Methacrylic acid
Page 3
October 1985

-------
VERSCHOERSN, X.  1177.  Handbook of Environmental Data on Organic
     Chemicals.  Van Nostrand Reinhold Co., Haw York.  659 pages

tftAST, R.B.r *d.  1981.  Handbook of Chemi«try and Physics.
     62nd «d.  CRC Press, Cleveland, Ohio.  2*332 pages
Methacrylic acid
Page 4
October 1985
                             33°

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                            METHANOL
Summary
     Methanol la highly toxic to humans when ingested or inhaled
as ft vapor.  It causes blindness, nausea, headaches, delirium,
and death.  In addition, inhalation of high doses had teratogenic
effects on the cardiovascular and urogenital systems of pregnant
rats.
CAS Number!  67-56-1
Chemical Formula:  CHjQH
IUPAC Name:  Methanol
Important Synonyms and Trade Names:  Methyl alcohol, wood alcohol

Chemical andLPhysical Properties
Molecular Weight:  32
Boiling Point:  64.5'C
Melting Points  -94*C
Specific Gravity:  0.791 at 2Q*C
Solubility in Water:  Miscible in water
Solubility in Organies:  Soluble in alcohol, acetone, ether,
                         benzene, and chloroform
Log Qctanol/Water Partition Coefficient:  -0.97 (calculated)
Vapor pressure:  96 ma If at 2Q*C
Vapor Density:  1.11
flash Point:  12*C (closed cup)

Transport and Pate
                        \
     No information on the transport and fate of methanol was
found in the sources reviewed.  However, based on the general
reactions of alcohols and the specific chemical and physical
properties of the material, likely transport and fate processes
can be determined.

Methanol
Page 1
October 1985
                                                              atas
                         391

-------
     Alcohols  are  very soluble  in water and therefore probably
 are  not  very volatile.  Some evaporation ii likely to occur,
 however,  especially lor a compound such as aethanol with a
 relatively  high  vapor pressure.  Oxidation is probably an im-
 portant  fate process in both surface water and the atmosphere.
 In soil,  metnanol  is probably biodegraded by soil microorganisms.


 Health Effects

     No  information on the carcinogenic!ty of aethanol was
 found in  the literature reviewed.  Several studies suggest
 that aethanol  may  have some autagenic activity.  High doses
 (26,000 mg/ra ) caused teratogenicity, including effects on
 the  cardiovascular and urogenital systems, when administered
 to pregnant rats for 7 hours.

     The  toxic effects of drinking aethanol, by mistaking it
 for  ethyl alcohol, are well known.  Ingestion of a few ounces
 of methanol aay  result in nausea; epigastric pain; vomiting;
 headaches; dizziness; delirium; visual disturbances, including
 blindness; and death (Treon 1963).  Similar effects have also
 been reported  after exposure to high levels of methanol vapor
 (Treon 1963).  The characteristic blindness that may develop
 in exposed humans  results from retinal destruction and degenera-
 tion of the optic nerve.  Metabolites of aethanol, particularly
 formaldehyde,  are believed to be responsible for this effect
 (Cornish  1980).  The metabolism of methanol in man also gives
 rise to formic acid, and this Is partly responsible for the
 severe acidosis  that develops in Intoxicated individuals (Cornish
 1980, Treon 1963).  However, chronic exposure to low levels
 of methanol, is not expected to have serious adverse health
 effects.


 Toxicitv  to Wildlife and Domestic Animals

     Methanol has a 48-hour LC.Q of 8,000 mg/liter in trout,
 and  the 24-hour LD. and L010Q values in creek chub are 8,000
 and  17,000 mg/liter, respectively.  No effects were seen in
Daphnia exposed to 10,000 mg/liter nor in a protozoa exposed
 to 1,250 mg/liter either.  Algae were not affected at levels
 of less than 10,000 mg/liter either.  The LC5Q of a saltwater
 species,  the brine shrimp, was 10,000 mg/litir.

     No data were available on the effects of methanol on domes-
 tic  animals or terrestrial wildlife in the literature reviewed.
Methanol
Page 2
October 198S

-------
Regulations and Standards

                          Is:   260 ao/a! TWA
                                                 Level
NIOSH Recommended Standards:    260 ag/a~  TWA
                             1,040 ag/sr  Ceiling
OSHA Standard  (air):  260 ag/m3 TWA

ACGIH Threshold Limit Values:  260 ag/a* TWA
                               325 ag/mj STEL


REFERENCES

AMERICAN CONFERENCE OF GOVERNMENTAL INDUSTRIAL HYGIENISTS (ACGIH) .
     1980.  Documentation of the Threshold Limit Values.  4th
     ed.  Cincinnati, Ohio.  488 pages

AMERICAN INDUSTRIAL HYGIENE ASSOCIATION (AIBA) .  1978.  Hygienic
     Guide Secies.  Methanol.  A1IA, Akron, Ohio

CORNISH, B.B.  1980*  Solvents and vapors.  In Doull, J.f Klaassen,
     C.D.  and Amdur, M.O., eds.  Casarett and Doull' s Toxicology.
     2nd ed.  Macmillan Publishing Co., New York.  Pp. 468-49$

LYMAN, W.J., REEHL, W.F. , and ROSENBLATT, D.B.  1982.  Handbook
     of Chemical Property Estimation Methods:  Environmental
     Behavior of Organic Compounds.  McGraw-Hill Book Co.,
     New York

TBS MERCK INDEX.  1976.  9th ed.  Windholz, M., ed.  Merck
     and Co., Rahway, New Jersey

NATIONAL INSTITUTE FOR OCCUPATIONAL SAFETY AND HEALTH (NIOSH).
     1984.  Registry of Toxic Effects of Chemical Substances.
     Data Base.  Washington, O.C.  July 1984

SAX, N.I.  1975.  Dangerous Properties of Industrial Materials.
     4th ed.  Van Nostrand Reinhold Co., New York.  1,258 pages

TKEON, J.F.  1963.  Alcohols.  In Patty, F.A., ed.  Industrial
     Hygiene and Toxicology.  2nd ed.  Interscience Publishers,
     New York.  Vol. 2, pp. 1409-1496

U.S. ENVIRONMENTAL PROTECTION AGENCY (USEPA) .  1979.  Water-
     Related Environmental Pate of 129 Priority Pollutants.
     Washington, D.C.  December 1979.  EPA 440/4-79-029
                        v
VZRSCRUEREH, K.  1977.  Handbook of Environmental Data on Organic
     Chemicals.  Van Nostrand Reinhold Co., New York.  659 pages

WE AST, R.E., ed.  1981.  Handbook of Chemistry and Physics.
     62nd ed.  CRC Press, Cleveland, Ohio.  2,332 pages


Methanol
Page 3
October 1985
                                                         Ammocimtmm

                         3S3

-------

-------
                         METHYL CHLORIDE
Summary

     Methyl chloride  is carcinogenic  in male mice, causing
tumors of the kidney  and  liver,  it was found to be autagenic
using the Aaes assay.  Methyl chloride has also been shown
to be teratogenlc; It produces heart  defects in the offspring
of exposed mice.  Exposure  to high concentrations adversely
affects the central nervous system, kidney, and liver  in humans,
CAS Number:  74-87-3

Chemical Formula:  CH.C1

IUPAC Name:  Chiororaethane

Important Synonyms and Trade Names;  Chloronethane, raonochloromethane



Chemical andPhysical yropertieji

Molecular Weight:  50.49 ;

Boiling Point*  -23.7*C

Melting Point.*  -t7»C

Specific Gravity:  0.9159 at 20*C

Solubility in Water:  6,450 to  7,250 ng/liter at 20*C

Solubility in Organicss  Miscible with  chloroform, ether, and
                         glacial acetic acid} soluble  in alcohol

Log Octanol/Water Partition Coefficienti  0.91


Transport and Fate

     Methyl chloride is a gas at normal environmental  tempera-
tures and therefore is unlikely to  remain in soil or water.
Experimental studies have found the half-life of methyl chloride
in agitated water to be 27 minutes.  Although this finding
may not be directly applicable  to natural waters,  it does suggest


Methyl chloride
Page 1
October 1985


                                                 Qcierrwit Amnocimtmm
Preceding page blank                               ^

-------
 rapid loss of the compound from water.   Socption  of  methyl
 chloride to soil or  sediment has not  been  studied; however,
 its relatively low log octanol/water  partition  coefficient
 suggests that partition occurs  primarily into air or water,

      The ujor route of environmental degradation of methyl
 chloride is probably through oxidation  in  the troposphere.
 At* this level of the atmosphere, the  methyl  chloride molecule
 is  attacked by hydroxyl radicals via  the mechanism of hydrogen
 abstraction.  The primary product is  forayl  chloride.
     •
              «

 Health  Effects

      Methyl chloride was found  to be  carcinogenic in male mice
 exposed to the  compound via inhalation  for a 2-year  period.
 A significantly increased incidence of  benign and malignant
 kidney  tumors was found in animals exposed to 2,100  mg/ro  .
 An  increased incidence of hepatocellular carcinomas  that was
 marginally significant was also found using  an  actuarial analysis
 of  the  data.  Negative results  for carcinogenelcity  for female
 nice  and male and fepale rats were obtained  in  the same study.
 Methyl  chloride has  been found  to be  nutagenlc  using the Ames
 assay,  with and without a aetabolic activating  system.  Methyl
 chloride has also been shown to be teratogenic  in mice, causing
 heart defects in fetuses.exposed in utero  at an airborne con-
 centration of IjOSO  mg/nr on gestation  days  f to  17.

      Methyl chloride is not considered  to  be highly  toxic.
 Repeated or prolonged human exposure  to sufficient concentrations
 (greater than 100 mg/nr)  can result in  central  nervous system
 (CNS) effects including blurred vision,  headache, nausea, loss
 of  coordination,  and personality changes.  Renal  and hepatic
 toxicity have also been reported in humans.  Animal  studies
 show  CNS effects and binding to aulfhydryl^containing cellular
 macromoiecules.   This latter effect interferes  with  metabolism
 and is  probably responsible for the observed tissue  toxicity.


 Toxieity to Wildlife and Domestic Animals

      The only information available on  the effects of methyl
 chloride in wildlife is an acute study  on  the bluegill that
 reported an LC«Q  value of 500 mg/liter  for this species.  Data
 on  the  other cnZorinatad methanes indicate that aquatic toxicity
 declines with decreased chlorination.   Thus  methyl chloride
 should  be  less  toxic than chloroform  or  carbon  tetrachloride,
 neither  of  which  had any effect on Daphnia magna  or  the fathead
minnow,  respectively,  during chronic  exposure to  3,400 jig/liter.
Ho  information  on the toxicity  of methyl chloride to terrestrial
 wildlife or domestic animals was found  in  the literature reviewed,
Methyl chloride
Page 2
October 1985

-------
Regulations and Standards

Ambient Water Quality Criteria  (USE?A)*

     Aquatic Life

     The available data are not adequate for establishing criteria.

     HunanHealth

     Estimates of the carcinogenic risks associated with lifetime
     exposure to various concentrations of halomethanes in
     water are:

         R i s k                    Concentration

     10"J                        1.9 ug/llter
     10.*                        °-19 Mg/liter
     10                          0.019 ug/liter

OSHA Standards:  210 mg/ml TWA
                 420 ag/aT Ceiling Level

ACGIH Threshold Limit Valuess  105 mg/m| TWA
                               205 mg/nr STEL


REFERENCES

AMERICAN CONFERENCE OF GOVERNMENTAL INDUSTRIAL HYGISNISTS (ACGIH}.
     1980.  Documentation of the Threshold Limit Values.  4th
     ed.  Cincinnati, Ohio.  488 pages

CHEMICAL INDUSTRY INSTITUTE OP TOXICOLOGY (CUT).  1981.  Final
     Report on Structural Teratogenicity Evaluations of Methyl
     Chloride in Rats and Mice After Inhaltion.  Prepared by
     Battelle Columbus Laboratories, April 30, 1981

CHEMICAL INDUSTRY INSTITUTE OP TOXICOLOGY (CUT).  1981.  Final
     Report on 24 Month Inhalation Study on Methyl Chloride.
     Prepared by Battelle Columbus Laboratories, December 31,
     1981

NATIONAL INSTITUTE FOR OCCUPATIONAL SAFETY AND 1EALTH (NIOSH).
     1983.  Registry of Toxic Effects of Chemical Substances.
     Data Base.  Washington, D.C.  October 1983

SIMMON, V.P., KOURANEN, X., and TAR DIP?, R.S.  19*»7.  Mutagenic
     activity of chemicals identified in drinking *ater.  In
     Scott, D., Bridges, B.A., and Sobels, F.H., eds.  'Progress
     In Genetic Toxicology.  Blsevier, Amsterdam.  Pp. 249-258
Methyl chloride
Page 3
October 1985

-------
U.S. ENVIRONMENTAL PROTECTION AGENCY  {USSPA).  1179.  Water-
     Related Environmental Fate of 129 Priority Pollutants.
     Vol. 2.  Washington, D.C.  December 1979.  EPA 440/4-79-029

O.S. ENVIRONMENTAL PROTECTION AGENCY  (USEPA).  1980.  JUabient
     Wattr Quality Criteria for ialotnethanes.  Office of Water
     Regulations and Standards, Criteria and Standards Division,
     Washington, D.C.  October 1980.  EPA 440/5-80-051

WEAST, R.E., ed.  1981.  Handbook of Chemistry and Physics.
     62nd ed.  CRC Press, Cleveland, Ohio.  2,332 pages
Methyl chloride
Page 4
October 198S
                                                                   • J

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                        METHYLffl^E  CHLORIDE
Summary.

     Methylene chloride increased the incidence of lung and
liver tumors and sarcomas in rats and nice.  It «•* found to
be mutagenic in bacterial test systems.  In humans, me thy 1 en e
chloride irritates the eyes, mucous membranes, and skin.  Exposure
to high levels adversely affects the central and peripheral
nervous systems and the heart.  In experimental animals, methylene
chloride is reported to cause kidney and liver damage, convulsions,
and paresis.                    .......


CAS Numberj  75-09-2

Chemical Formula:  CH^Clj

IUPAC Name:  Dichloromethane

Important Synonyms and Trade Names:  Methylene dichloride, methane
                                     dichloride


Chemical and Physical Properties

Molecular Weight:  84.93

Boiling Pointi  40*C

Melting Point:  -95.1»C

Specific Gravity:  1.3266 at 20*C

Solubility  in Water:  13,200-20,000 mg/liter at 2S*C

Solubility  in Organics:  Miscible with alcohol and ether

Log Octanol/Water Partition Coefficient:   1.25

Vapor Pressure:  362.4 mm Bg at 20*C

Vapor Density:  2.93
                        \

Transport and Fate

     Volatilization to the atmosphere appears to be the major
mechanism for removal of methylene chloride from aquatic systems
Methylene chloride
Page 1
October 1985
                                                             i«tt«»

-------
 and  its primary environmental  transport process  (USEPA  1979).
 Photooxidation  in the troposphere appears to be  the dominant
 environmental fate of aethylene chloride.  Once  in the  troposphere,
 the  compound  is attacked by hydroxyl  radicals, resulting in
 the  formation of carbon dioxide, and  to a lesser extent/ carbon
 aonoxide  and phosgene.  Phosgene is readily hydrolyzed  to HC1
 and  CO..  About on* percent of  tropospheric methylene chloride
 would  Be  expected to reach the stratosphere where it would
 probably  undergo photodissociation resulting froa interaction
 with high energy ultraviolet radiation.  Aerial  transport of
 nethylene chloride is partly responsible for its relatively
 wide environmental distribution.  Atmospheric aethylene chloride
 may  be returned to the earth in precipitation.

     Photolysis, oxidation, and hydrolysis do not appear to
 be significant environmental fate processes for  methylene chlor-
 ide, and  there  is no evidence to suggest that either adsorption
 or bioaccumulatlon are important fate processes  for this chem-
 ical.  Although nethylene chloride is potentially biodegradable,
 especially by acclimatized microorganisms, biodegradation prob-
 ably only occurs at a very slow rate.


 Health Effects

     Methylene chloride is currently  under review by the National
 Toxicology Program (NTP 1984, USEPA 1985).  Preliminary results
 indicate  that it. produced an increased incidence of lung and
 liver tumors in mice and mammary tumors in female and male
 rats.  In a chronic inhalation study, male rats  exhibited an
 increased incidence of sarcomas in the ventral neck region
 (Burek et al.  1984).  However, the authors suggested that
 the  relevance and toxicological significance of  this finding
 were uncertain in light of available  toxlcity data.  Methylene
 chloride  is reported to be mutagenic  in bacterial test systems.
 It also has produced positive results in th« Fischer rat embryo
 cell transformation test.  However, it has been  suggested that
 the  observed cell-transforming capability may have been due
 to impurities in the test material.  There is no conclusive
 evidence  that aethylene chloride can  produce teratogenic effects.

     In humans,  direct contact with aethylene chloride produces
 eye, respiratory passage, and skin irritation (USEPA 1985).
 Mild poisonings due to inhalation exposure produce somnolence,
 lassitude, numbness and tingling of the limbs, anorexia, and
 lightheadedness, followed by rapid and coaplete  recovery.
More severe poisonings generally involve correspondingly greater
disturbances of the central and peripheral nervous systems.
Methylene chloride also has acute toxic effects  on the heart,
 including the induction of arrhythmia.  Fatalities reportedly
Methylene chloride
Page 2
October 1985

-------
due to methylene chloride exposure have been attributed  to
cardiac Injury and heart failure.  Methylene chloride  is metabolized
to carbon monoxide in vivo, and levels of carboxyhemoglobin
in the blood are elevated after acute exposures.  In experimental
animals, methylene chloride is reported to cause kidney and
liver damage, convulsions* and distal paresis.  An
value of 2,136 «g/kg, and an inhalation LCB<1 value
30 min are reported for the rat.
                                          'SO
oral LD
of 88,0
                                               mg/rn /
Toxicity to Wildlife andDomestic Animals

     Very little information concerning the toxic ity of nethylene
chloride to domestic animals and wildlife exists (OSEPA 1980).
Acute values for the freshwater species Paphnia aagna, the
fathead minnow, and the bluegill are 224,000, 193,000, and
224,000 pg/liter, respectively.  Acute values for the saltwater
species, mysid shrimp and sheepshead minnow, are 256,000 and
331,000 ug/liter, respectively.  Ho data concerning chronic
toxicity are available.  The 96-hour SC_Q values for both freshwater
and saltwater algae are greater than the highest test concentration,
662,000 Mi/liter.


Regulat ions and Standards

Ambient Hater Quality Criteria  (USEPA) s

     Aquatic Life    -  :

     The available data, are not adequate for establishing criteria.


     Human Health

     Criterion:  12.4 mg/liter  (foe protection against the
                 noncarcinogenic effects of methylene chloride)

CAG Unit, tisk  (DSEPA):  1.4xlO~2(ag/kg/day>"*

NIOSH Recommended Standards!

     261 mg/m3 TWA in the presence of no more than 9.9 mg/ra3 of CO
     1,73? mg/m /IS min Peak Concentration
OSHA Standards
s   1,737 mg/ul TWA
   3,474 »g/m? Ceiling
                                     Level
                 6,948 mg/m  Peak Concentration  (5 ain in any 3 hr)
ACGIH Threshold Limit Values:  3SO mg/m3 TWA
                               1,740 «f/»  ST£L
Nethylene chloride
Page 3
October 1985
                                                  [Owrwit Ammocmvmn

-------
 REFERENCES

 AMERICAN CONFERENCE OF GOVERNMENTAL INDUSTRIAL 1YGIENISTS  (ACGIH).
      1990,  Documentation of the Threshold Limit Values.   4th ed.
      Cincinnati, Ohio.  488 pages

 BUREK, J.D.I, NITSCHKB, K.D., BELL, T. J., WACKBRLE, D,L. , CHILDS,
      R.C., BEYER, J.E., DITTENBER, D.A., RAMPY, L.W., and MCKENNA,
      M.J.  1984.  Methylenc chlorides A two-year inhalation
      toxicity and oncogenicity study in cats and hamsters.
      Fundam. Appl. Toxieol. 4:30-47

 NATIONAL INSTITUTE FOR OCCUPATIONAL SAFETY AND HEALTH (NIOSH).
      1976.  Criteria foe a Recommended  Standard—Occupational
      Exposure to Methylene Chloride.  March 1976.  DHEW Publi-
      cation NO.  (HIOSH) 76-138

 NATIONAL INSTITUTE FDR OCCUPATIONAL SAFETY AND HEALTH (NIOSH) .
      1983.  Registry of Toxic Effects of Chemical Substances.
      Data. Base.  Washington, D.C.

 NATIONAL TOXICOLOGY PROGRAM (NTP).  1984.  NTP Technical Report
      on the Toxicology and Carcinogenesis Studies of Methylene
      Chloride (CAS No. 75-09-2} in F344/N Rats and 86C3F, Mice
      (Inhalation Studies) NTP Technical Report No. 291. Tie search
      Triangle Park, North Carolina..  OSDHHS (NIB) Publication
      No. 85-2562

 SAX,  N.I.  1975.  Dangerous Properties  of Industrial Materials.
      4th ed.  Van Nostrand Reinhold Co., New York.  1,258 pages

 U.S.  ENVIRONMENTAL PROTECTION AGENCY (US2PA).  1979.  Water-
      Related Environmental Fate of 129  Priority Pollutants.
      Washington, D.C.  December 1979.   EPA 440/4-79-029

 U.S.  ENVIRONMENTAL PROTECTION AGENCY (USEPA).  1980.  Ambient
      Water Quality Criteria for Halomethanes.  Office of Water
      Regulations and Standards, Criteria and Standards  Division,
      Washington, D.C.  October 1980.  EPA 440/5-80-051

 U.S.  ENVIRONMENTAL PROTECTION AGENCY (USEPA).  1984.  Health      '
      Effects Assessment for Methylene Chloride .  Environmental
      Criteria and Assessment Office, Cincinnati, Ohio.   September
      1984.  ECAO-CIN-H028  (Final Draft)

 U.S.  ENVIRONMENTAL PROTECTION AGENCY (USEPA).  1985.  Health
      Assessment Document for Chloroform.  Office of Health.
      and Environmental Assessment, Washington, D.C.  September
      1985.  EPA 600/8-84/004F

WEAST, R.S.r td.  1981.  Handbook of Chemistry and Physics.
      62nd ed.  CRC Preis, Cleveland, Ohio.  2,332 pages


 Methylene chloride
 Page  4
 October 1985

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                       METHYL ETHYL KSTONE
Summary
     Methyl ethyl ketone  (NEK) retarded fetal development and
had son* teratogenie effects in the offspring of exposed pregnant
cats.  At high doses* it  affects the nervous system and irritates
the eyes, mucous membranes, and skin.  In addition, methyl
ethyl ketone strongly potentiates the neurotoxie effects of
n-hexane and n-hexaraone.


CAS Number!  78-93-3

Chemical Formulas  C^HgO

TUPAC Name s  Bu tanone

Important Synonyms and Trade Names:  Ethyl methyl ketone , H£K,
                                     2-butanone


Chemical and Physical Properties

Molecular Weights" 72.1   --•'---               -

lolling Points  7t.6»C         u  '7

Melting Points  -86.3S*C

Specific Gravityj  0.805  at 20«C

Solubility in Waters  Very soluble in water

Solubility in Organics:   Miscible with alcohol, ether, benzene
                          and acetone

Log Octanol/Water Partition Coefficients  0.29

Vapor Pressures  71.2 ma  eg at 20*C

Vapor Density s  2.41                  /

Flash Points  2*C
                       «k

Transport and Fate

     Very limited information on the transport and fate of
•ethyl ethyl, ketone was found in the literature reviewed.
However, ke tones in general are probably not very persistent.


Methyl ethyl ketone
Page 1
October 19S5

-------
Methyl  ethyl  ketont  has a high  vapor pressure  and  therefore
would be expected  to volatilize readily.  However*  because
of  its  high water  solubility, volatilization is probably  limited
in  aquatic systems or wet soil.  Once  in the atmosphere it is
apparently oxidized  (Hoare and  Whytock  1167).  Methyl ethyl
ketone  has i  low octanol water  partition coefficient and  there-
fore is probably not readily adsorbed.  Biodegradation is prob-
ably the predominant fate of methyl ethyl ketone in the environ-
ment because  of its  aliphatic nature.


Health  Effects

     Methyl ethyl  ketone has not been  adequately tested for
carcinogenicity and  has produced only equivocal evidence  of
mutagenieity  in a  few bacterial assays.  Schwetz et al. (1974)
reported that HER  caused retarded fetal development and some
teratogenic effects  (acaudii, imperforate anus, and brachygna-
thia) at air  concentrations of  3,000 ppo  {approximately
f»000 mg/m ).  Methyl ethyl ketone is of relatively low toxicity
but at  high doses  affects the nervous system and causes irri-
tation  of the eyes,  nose, and skin..  The oral LD-. value  for
the rat was 2,750 ag/kg.                        *°

     Although MEK  is not strongly neurotoxic alone, it apparently
strongly potentiates the neurotoxicity of n-hexane and n-hexanone
(methyl n-isobutyl ketone).


Toxicity to Wildlife and Domestic Animals

     Only limited  information was available on the toxicity
of  methyl ethyl ketone to wildlife.  LC,Q concentrations  for
two freshwater fishes were around 5,600 pg/liter (Turnball
et  al.  1954;  Wallen  et al. 1957).  MEK was toxic to brine shrimp
at I»C5Q levels of  1950 nig/liter.

     HO information on the toxicity of MEK to  terrestrial wild-
life or domestic animals was found in the .literature reviewed.


Regulations and Standards

NIOSH Recommended Standard:  590 mg/m  TWA

OSHA Standard (air):  ZOO ppm (590 mg/m3) TWA
Methyl ethyl ketone
Page 2
October 1985

-------
 REFERENCES

 AMERICAN CONFERENCE  Of  GOVERNMENTAL  INDUSTRIAL  IYGISNISTS  (ACGIH)
      1980.  Doeuaentation  of  the Threshold Limit Values.   4th  •
      ed.  Cincinnati, Ohio.   488 pages

 HOARE,  D.E.,  and  WIYTOCK,  D.A.  1167.  Photooxidatton of methyl
      ethyl ketone vapor. Can. J. Chem. 45:2741-2748

 NATIONAL INSTITUTE FOR  OCCUPATIONAL  SAFETY AND  HEALTH (NIOSH).
      1978.   Criteria for a Recommended Standard—occupational
      Exposure to  Ketones.  Washington, D.C.  SHEW Publication
      NO. (NIOSH)  78-173

 SCHWETZ* B.A., LEONG, B.K.J., and GEHRING, P.J.  1974.  Embryo-
      and fetotoxicity of inhaled carbon tetrachloride,  1,1-di-
      ehloroethane and methyl  ethyl ketone in rats.  Toxieol.
      Appl.  Pharaacol. 23:452-464
 TURNB'JLL,  H.,  DeMANN, J.G., and WESTON, R.F.  1954.  Toxicity
      of  various refinery wait* materials to freshwater  fish.
      Ind.  Eng. Chem. 46:324

 D.S.  ENVIRONMENTAL PROTECTION AGENCY (USEPA).   1984.  Health
      Effects  Assessment foe Methyl Ethyl Ketcne.  Environmental
      Criteria and Assessment Office, Cincinnati, Ohio.  September
      1984.  ECAO-CIN-H003   (Final Draft)

 WALLEN,  I.E.,  GREER, W.C., and LASATER, R.  1957.  Tozicity
      to  Gambusia  affinis of certain  pur* chemicals in turbid
               Sewage Ind. Wastes 295195-711
Methyl ethyl ketone
Page 3
October 1985

-------

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                      METHYL ISQIUTXL KETONE
Summary
     Methyl isobutyl ketone produced kidney damage in exposed
rats.  In human*, exposure has produced headaches, nausea, vomit-
ing, and eye irritation.
CAS Number:  108-10-1
Chemical Formula:   (CH,)-CHCH-COCH,
IUPAC Namei  4-Methyl-2-pentanone
Important Synonyms and Trade Names:  Hexone, isobutyl methyl
                                     ketone, isopropyl acetone,
                                     MIX, and MIBK
Chemical and Physical Properties
Molecular Height:  100.2
Boiling Point:  117*C
Melting Points  -84.7*C
Specific Gravity:  0.7978 at 20*C
Solubility in Water:  Soluble
Solubility in Organics:  Soluble in chloroform, alcohol, ether,
                         acetone, benzene, and many other organic
                         solvents
Log Octanol/Water Partition Coefficient:  1.18
Vapor Pressure:  15 m Hg at 20*C
Vapor Density:  3.45
Flash Pointt  23*C
Transport and Fate
     Very limited information on the transport and fate of methyl
isobutyl ketone (MIBK) was found in the literature reviewed.
However, ketones in general are probably not very persistent.
Methyl isobutyl ketone would be expected to volatilize fairly

Methyl isobutyl ketone
Page 1
October 1985
Preceding page blank
                                                   =l-m*nc

-------
 volatilixation Scorn wet  environaents  it probably Halted.  Once
 in the atmosphere it is  apparently oxidized.  Methyl  isobutyl
 ketone has a low oetanol/water partition coefficient  and there-
 fore is probably not readily  adsorbed.  Biodegradation is probably
 the predoaiaant fate of  methyl iaobutyl ketone in the environment.
 Evidence of thii is provided  by  the biological oxygen demand
 value for Methyl iiobutyl  ketone, which was 691 of the theoretical
 value after 20 days at 2Q*C,


 Health Iffecta

      Ho studies on the carcinogenic! tyr mutagenicity, reproductive
 toxicity or teratogenicity of methyl  isobutyl ketone were found
 in the literature reviewed.  Kidney damage was observed in
 rats  exposed to 400 ag/a  of MI3K for 2 weeks but the damage
 appeared to be reversible.  Methyl isobutyl ketone caused head-
 ache,  nausea,  vomiting,  and eye  irritation in a number of workers
 exposed to concentrations  of  200 to 2,000 ag/a .  The oral
      for NIBK  in the rat was  2,080 ag/kg.
Toxieity  to Wildlife and Domestic Animals

     The  only study on the toxicity of methyl isobutyl ketone to
wildlife  reported that the TL.g for brine shrimp was 1,230 ag/liter
MIBK is probably also not very toxic to other aquatic species
or to terrestrial animals.


Regulations and Standards

tifOSH Recommended Standard i  200 ag/m  TWA

OSHA Standard (air):  400 ag/a3 TWA

ACGIH Threshold Limit Value* r  205 ag/a| TWA
                               300 ag/a4 STSL


REFERENCES

AMERICAN  CONFERENCE Of GOVERNMENTAL INDUSTRIAL HYGIENISTS (ACGIH) .
     1980.  Documentation of the Threshold Limit Values.  4th
     •d.  Cincinnati, Ohio.  488 pages

NATIONAL  INSTITUTE FOR OCCUPATIONAL SAFETY AND HEALTH (NIOSH) .
     1978.  Criteria for a Recommended Standard— Occupational
     Exposure to Ketones.  Washington, D.C.  DHEW Publication
     Mo.  (NIOSH) 78-173
Nethyl isobutyl ketone
Pig* 2
October 1985
                                 3?*

-------
NATIONAL INSTITUTE FOR OCCUPATIONAL SAFETY AND IEALTH  (NXOSH).
     1983.  Rtgiitry of Toxic Effects of Chemical Substances.
     Data Base.  Washington, B.C.  October 1983

VERSCHUEREN, K.  1977.  Handbook of Environmental Data on Organic
     Chemicals.  Van Hostrand Reinhold Co./ New York.  659 pages

WEAST, R.E., ed.  1981.  Handbook of Chemistry and Physics.
     62nd ed.  CRC press, Cleveland, Ohio.  2,332 pages
Methyl isobutyl lie tone
Page 3
October 1985
                                                                  20,'

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                         METHYL PAKAT1ION
 Summary
     Methyl parathion was enbryotoxic, decreased reproductive
potential f and lowered the survival rate ol offspring when
administered to experimental animals.  Exposure also inhibits
the activity of cholinesterase.  wild birds are particularly
susceptible to the toxic effects of methyl parathion.


CAS Number:  298-00-0

Chemical Formula:  CgI.~liO.PS

IUPAC Name: OjO-Dimethyl-o/p-Nitrophenylphosphorothioate

Important Synonyms and Trade Naaess  Metaphor , Wofatox


Chemical and Physical Properties

Molecular Weight:  263.23

Boiling Point:  Thermally unstable; cannot be heated to normal
                boiling point

Melting Points  3?-3S*C

Specific Gravityi  1.358 at 20*C

Solubility in Water:  SO *g/liter at 20*C

Solubility in Organics:  Soluble in moat organic solvents

Vapor Pressures  9.7 x 10~* sm Hg at 20 *C


T r an ago r t and F ate

     Methyl parathion is broken down quickly under environmental
conditions! primarily by hydrolysis.  Initial decomposition
products in soil ar* p-nitrophenol and dimethylthiophosphoric
acid.  Methyl parathion will volatilize from soil and water.
In the atmosphere, the sulfur atom is replaced by oxygen to
yield methyl paraoxon, which is rapidly hydrolyzed.  Sioaccuau-
lation is probably not an important fate process for methyl
parathion and although adsorption to soils may occur, it is
also probably not an important fate process because of -the
rapid hydrolysis of the chemical.  Methyl parathion is unlikely
to leach through soil and enter the groundwater because of
its low water solubility and short persistence.


Methyl parathion
page 1
October 198S
                                                              CMKM
 Preceding page blank


-------
 Health Effects

      Mtthyl  parathion  was  not  carcinogenic when  administered
 orally to rats and  mice  (MCI 1979),  and was not  smtagenie or
 only marginally positive foe autagenieity in numerous assays
 (Chen et  al.  1981). Mtthyl ptrathion did induce sister chroraatid
 exchange  and caused eell cycle delay, however.   It does not
 appear to be a teratogen but is a  reproductive toiin causing
 decreased reproductive potential,  decreased survival off off-
 spring, and  eabryotoxicity.

      Methyl  parathion  is converted in vivo to the oxygen analog,
 •ethyl paraoxon, which is  responsible for its primary toxic
 effect:   cholinesterase  inhibition.  Only one subchronic study
 was  available on methyl parathion.   This showed  that continuous
 doses produced a steady decrease in  enzyme activity but that
 upon  cessation of dosing the animals recovered fairly quickly.
 Methyl parathion is Quite  acutely  toxic, with an oral LD__
 value in,  rats of about 15  mg/kg.                        5U


 Toxicitv  to Wildlife and Domestic  Animals

      Methyl  parathion  was  Moderately toxic to freshwater and
 saltwater  fish, with LC5Q  values ranging from 19,000 to 75,000
 Mi/liter.  However*  it fas quite toxic to invertebrate species,
 with  LC.Q  values between 2 and 50  tig/liter.  The pesticide
 did not'appear  to affect rodent populations after field appli-
 cation but did  cause some  mortality  in pheasant  populations.
 Laboratory studies  have also indicated that wild birds are
 quite susceptible to the toxic effects of methyl parathion;
 quail were more sensitive  than pheasants or ducks.  Methyl
 parathion  was also  quite toxic to  nontarget insects.  No reports
 of toxic effects on domestic aniaals were reported in the litera-
 ture  reviewed.  Methyl parathion is  fairly quickly metabolized
 in vivo to nontoxie products and is  only slightly lipid soluble,
 and therefore is not expected  to bi©accumulate or biomagnify
 in aniaals.


Regulations and Standards

 NIOSH  Recommended Standard (air)i  0.2 mg/m3 TWA


 REFERENCES

CHEN, I.I., HSUZH,  J.L.", SIRIANNI, S.R., and HUONG, C.C.  1981.
      Induction of sister-chrooatid exchanges and cell cycle
     delay in cultured mammalian cells treated with eight organo-
      phosphata pesticides.  Mutat. Res. 88i307-316
Methyl parathion
Page 2
October 1985

-------
 NATIONAL CANCER  INSTITUTE  (NCI).   1979.  Bioassay of Methyl
      Parathion for Possible Carcinogenicity.  CAS No. 298-00-0,
      NCI Carcinogenesis Technical  Report Series Ho. 157.  Wash-
      ington, D.C.  DREW Publication No.  (NIB) 79-1713

 NATIONAL INSTITUTE FOR OCCUPATIONAL SAFETY AND HEALTH (NIOSH).
      1984.  Registry of Toxic Effects of Chemical Substances,
      Data Base.  Washington, D.C.  January 1964

 U.S.  ENVIRONMENTAL PROTECTION AGENCY  (OSEPA).  1975.  Initial
      Scientific  and Miniecononie Review of Methyl Parathion.
      Substitute  Chemical Program,  Washington, D.C.  EPA 540/1-
      75-004
VERSCHUEREN, K.
     Chemicals.
     pages
1977.  Handbook of Environmental Data on Organic
Van Nostrand Reinhold Co., New York.  6S9
WEAST, R.E., ed.  1981.  Handbook of Chemistry and Physics.
      62nd ed.  CRC Press, Cleveland, Ohio.  2,332 pages
Methyl parathion
Pag* 3
October 1985

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                           NAPHTHALENE
Summary
     Naphthalene retarded cranial ossification and heart develop-
ment in  the offspring of exposed pregnant rats.  Inhalation
exposure caused nausea, headache, and optic and kidney damage
in humans and experiaental animals.  Oral administration produced
cataracts in rabbits and Induced changes in motor activity
in rats  and mice.  Exposure to high doses of naphthalene cause
severe hemolytic effects.


CAS Number:  91-20-3

Chemical Formula:  C.ftHfl
                    Aw O

IUPAC Name:  Naphthalene

Important Synonyms and Trade Names:  Naphthene, tar camphor,
                                     moth balls


Chemical and Physical Properties

Molecular Weight:  128.16

Boiling  Points  217.I*C

Melting  Point;  80.2*C

Specific Gravity:  1.1S2 at 20*C

Solubility in Water:  34.4 ing/liter at 25*C

Solubility in Organics:  Soluble in alcohol, ether, acetone,
                         and benzene

Log Octanol/Water Partition Coefficient:  3.3?

Vapor Pressure:  0.08? an Bg at 2S*G

Vapor Densityi  4.42
                         ^

Transport and Fate

     Environmental transport and fate is largely .inferred from
data for polycyclic aromatic hydrocarbons (PAHs) in general,
because  specific information foe naphthalene is lacking.  Rapid,
direct photolysis of naphthalene to quinones may be an important


naphthalene
Page 1
October  1985
Preceding page blank

-------
 process  in  surface  waters.  Oxidation  is probably  too  slow  to
 be  a  significant environmental process.  However,  data for
 •one  PAHs suggest that oxidation by  chlorine or  ozone  nay be a
 significant fat* process when these  oxidants are available  insuf-
 ficient  quantity.   Volatilization nay  play a rol*  in trans-
 port  depending  on mixing rates in both the water column and air
 column.  For naphthalene, adsorption is the aoit important
 aquatic  transport process.  Consideration of its log oetanol/water
 partition coefficient and of the behavior of other PAHs indicate
 that  naphthalene can be strongly adsorbed onto suspended and
 sedimentary particulate matter, especially participates high
 in  organic  content.  Dominance of volatilization or absorp-
 tion  as  a transport process is directly related  to environmental
 conditions.   It is  likely that this  compound can be readily
 transported as  adsorbed aatter or suspended participates in
 air or water.

      Based  on information concerning related compounds, it
 is  likely that  bioaecumulation of naphthalene is short term,
 especially  for  vertebrates.  Although  this compound is rapidly
 accumulated,  it also is rapidly metabolized and  excreted, and
 consequently bioaccuaulation is not  considered an  important
 fate  process.  Naphthalene can be metabolized by multicellular
 organisms and degraded by microbes.  Degradation by mammals
 is  likely to be incomplete, with paten compound  and the meta-
 bolites  being excreted by the urinary  system.  Biodegradation
 by microorganisms is probably the ultimate fate  process for
 naphthalene.  Biodegradation generally appears to  be more effi-
 cient in soil than  in aquatic systems.  However, experimental
 data  indicate that  biodegradation may  be more important in
 those aquatic systems which are chronically affected by PAH
 contamination.

      Atmospheric transport of PAHs can occur, and  these materials
 can be returned to aquatic and terrestrial systems by  vet and
 dry deposition.  Some PAHs may enter surface and groundvaters
 by leaching  from polluted soils.


 Health Effects

     there  ace no epidemi©logical or case studies  available
 suggesting  that naphthalene is carcinogenic in humans.  This
 compound Is  not generally considered to be carcinogenic in
 experimental animals.  However, there  is equivocal evidence
 suggesting  weak carcinogenic activity  in rats after subcutaneous
 injection.   Naphthalene Is reported  to produce DNA damage in
mice  after  intraperitoneal injection.  Retarded  cranial ossi-
 fication and  heart development are reported among  offspring
of rats  injected iatraperitoneally with naphthalene on days 1
 to IS of gestation.
naphthalene
Page 2
October 1985

-------
     little Information conctcning acute and chronic  toxic
effects is available.  Inhalation exposure to naphthalene may
cause headache, loss of appetite, nausea, and kidney  damage
in humans and experimental animals.  Acute hemolytic  effects
are reportedly caused by ingestion or inhalation of relatively
large quantities of naphthalene.  Optical neuritis, injuries
to the cornea, and opacities of the lens also may result after
inhalation exposure or ingestion.  Naphthalene is a mild eye
irritant in rabbits, and cataracts can be induced after oral
administration.  Application to the skin produces erythema
and slight edema in rabbits.  Somnolence and changes  in motor
activity are observed after ingestion of naphthalene  by rats
and mice.  Oral LD5fl values of 1,250 mg/kg and 580 mg/kg are
reported for the cat and the mouse, respectively.


Toxicity to Wildlife and Domestic Animals

     The median effect concentrations for freshwater  inverte-
brate species and three fish species are all reported to be
greater than 2,300 ug/liter.  Acute values reported for saltwater
polychaete, oyster, and shrimp species are all greater than
2,350 Mg/liter.  A chronic value of 620 uf/liter and  an acute-
chronic ratio of 11 is reported for the fathead minnow, a fresh-
water species.  Mo chronic values are available for saltwater
species.  Freshwater algae appear to be less sensitive to the
effects of naphthalene than animal species.  Ho information
concerning saltwater plant species is available.  The weighted
average bioconcentration factor for the edible portion of all
freshwater and estuarine aquatic organisms consumed by Americans
is 10.5.

                                          *
Regulations and Standards

Ambient Water Quality Criteria (USEPA)i

     The available data are not adequate for establishing criteria,

OSHA standard:  50 »g/»3 TWA

ACGIH Threshold Limit Values:  50 mg/mij TWA
                               75 mg/m4 STEL


REFERENCES

AMERICAN CONFERENCE OP GOVERNMENTAL INDUSTRIAL HYGIENISTS  (ACGIH).
     1980.  Documentation of the Threshold Limit Values. * 4th
     ed.  Cincinnati, Ohio.  488 pages
Naphthalene
fage 3
October 1985

-------
 DOULL,  J.»  JCLAASSEN,  C.D.,  and AMDUR, M.O.   1980.  Casarett
      Doull'i Toxicology:  Th* Basic  Science  of Poisons.   2nd
      *d.  Macmillan Publishing Co.,  Hew fork.  778
 NATIONAL  INSTITUTE FOR OCCUPATIONAL SAFETY AND HEALTH  (NIOSH) .
      If 84.   Registry of Toxic Effects of Chemical Substances.
      Data Base.  Washington, D.C.  April 1984

 SAX,  N.I.  1975.  Dangerous Properties of Industrial Materials.
      4th  *d.  Van Nostrand Reinhold Co., New fork.  1,258 pages

 U.S.  ENVIRONMENTAL PROTECTION AGENCY  (USEPA) ,  1979.  Water-
      Related Environmental Fat* of 129 Priority Pollutants.
      Washington, D.C.  December 1979.  EPA 440/4-79-029

 U.S.  ENVIRONMENTAL PROTECTION AGENCY  (DSEPA) .  1980.  Ambient
      Hater  Quality Criteria for Naphthalene.  Office of Hater
      Regulations and Standards, Criteria and standards Division,
      Washington, D.C. 'October 1980.  EPA 440/5-80-059

 U.S.  ENVIRONMENTAL PROTECTION AGENCY  ( USEPA} .  1984.  Health
      Effects Assessment for Naphthalene.'  Environmental Criteria
      and  Assessment Office, Cincinnati, Ohio.   September 1984.
      ECAO-CIN-H014  (Final Draft)

 WEAST,  R.S. , ad.  1981.  Handbook of Chemistry and Physics.
      62nd ed.  CRC Press, Cleveland, Ohio.  2332 pages
Naphthalene
Pag* 4
October 1985

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                              NICKEL
Summary
     In • number of epidemioiogical studies, occupational ex-
posure to nickel compounds has been associated with excess
cancer of the lung and nasal cavity.  In addition, inhalation
exposure to nickel subsulfide and nickel carbonyl has been
shown to cause cancer in rats, while studies off other nickel
compounds administered to animals by other routes have reported
carcinogenic effects as well.  Several nickel compounds are
mutagenie and can cause cell transformation.  In humans, nickel
and nickel compounds can cause a sensitization dermatitis.
The chronic toxicity of nickel to aquatic organisms is high.


Back ground Information

     The commonly occurring valences of nickel are 0, +1, +2,
and +3, with +4 rarely encountered.  Although elemental nickel
is seldom found in nature and is not soluble in water, many
nickel compounds are highly soluble in water.  Nickel is alnost
always found in the divalent oxidation state in aquatic systems.

CAS Number:  7440-02-0

Chemical formula:  Hi

I DP AC Name*.  Nickel


Chemical and Physical Properties

Atomic Weight:  51.71

Boiling Pointt  2,?32*C

Meltdng Point!  1,453*C

Specific Gravityi  8.902 at 2S*C

Solubility in Water:  Insoluble? some salts are soluble

Solubility in Organics:  Depends on the properties of the specific
                        vnickel salt

Vapor Pressure:  1 mm Eg at 1,810*C
Nickel
Page 1
October 1985

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 Transport  and /ate

      Nickel  i*  • highly  mobile  metal  in  aquatic  systems because
 •any nickel  compound!  are  highly  soluble in water.  However,
 the insoluble sulfide  is formed under  reducing conditions  and
 in  the  presence  of  sulfur.  Above pH  9,  precipitation of the
 hydroxide  or carbonate exhibits some  control en  nickel nobility.
 In  aerobic environments  below pH  9, soluble compounds are  formed
 with hydroxide,  carbonate,  sulfate, and  organic  ligands.

      In natural*  unpolluted waters, sorption and coprecipitation
 processes  involving hydrous iron  and manganese oxides are  prob-
 ably at least moderately effective  in  limiting the mobility
 of  nickel.   Zn more organic-rich, polluted waters, it appears
 that little  sorption of  nickel  is likely.  The lack of other
 controls on  nickel mobility probably makes incorporation into
 bed sediments an important fate of  nickel in surface waters.
 However, much of the nickel entering  the aquatic environment
 will be transported to the  oceans.

      In general,  nickel  is  not  accumulated in significant  amounts
 by  aquatic organisms.  Bioconcentration  factors  are usually on
 the order of 100 to 1,000.  Uptake  of  nickel from the soil
 by  plants  can also occur.  Photolysis, volatilization, and
 bio transformation are  not  important environmental fate processes
 for nickel.  lowever,  atmospheric transport of nickel and  nickel
 compounds on particulate matter can occur.


 Health  Effects

      There is extensive  epidemiological  evidence indicating
 excess  cancer of  the lung  and nasal cavity for workers at  nickel
 refineries and smelters, and weaker evidence for excess risk
 in  workers at nickel electroplating and  polishing operations.
 Respiratory  tract cancers  have  occurred  in excess at industrial
 facilities that  are metallurgically diverse in their operations.
 The nickel compounds that  have  been implicated as having car-
 cinogenic potential are  insoluble dusts  of nickel subsulfide
 and nickel oxides, the vapor of nickel carbonyl, and soluble
 aerosols of  nickel sulf ate, nitrate, or  chloride.  Inhalation
 studies with experimental animals suggest that nickel subsulfide
 and nickel carbonyl are  carcinogenic in  rats.  Evidence for the
 carcinogenicity  of nickel metal and other compounds is relatively
 weak  or  inconclusive.  Studies  with experimental animals indicate
 that  nickel  compounds  can also  produce various types of malignant
 tumors  in experimental animals  after administration by other
 routes,  including subcutaneous, intramuscular, implantation,
 intravenous, intrarenal, and intrapleural.  Carcinogenic poten-
 tial  is  not  strongly dependent  on route  or site  of administra-
 tion  but appears  to be inversely  related to the  solubility
of  the  compounds  in aqueous media.  Insoluble compounds, such


Rickel
Page  2
October  1985

-------
as nickel dust, nickel  sulfide, nickel carbonate* nickel oxide,
nickel carbonyl, and nickelocene  are carcinogenic, whereas
soluble nickel  salts such as  nickel chloride, nickel  sulfate,
and nickel ammonium sulfate,  are  not.

     Mammalian  cell transformation data,  indicate that several
nickel compounds are nutagenic and can cause chromosomal altera-
tions.  The available information is inadequate for assessing
teratogenic and reproductive  effects of  nickel in humans and
experimental animals*

     Dermatitis and other deraatological effects are  the most
frequent effects of exposure  to nickel and nickel-containing
compounds.  The dermatitis  is a sensitization reaction.  Most
information regarding acute toxicity of  nickel involves inha-
lation exposure to nickel carbonyl.  Clinical manifestations
of acute poisoning include both immediate and delayed symptoms.
Acute chemical pneumonitis  is.produced,  and death may occur at
exposures of 30 ppa (10? mg/arj for 30 minutes.  Rhinitis,
nasal sinusitis, and nasal mucosal injury are among the effects
reported among workers  chronically exposed to various nickel
compounds.  Studies with experimental animals suggest that
nickel and nickel compounds have  relatively low acute and chronic
oral toxicity.


Toxieity to Wildlife and Domestic Animals

     In freshwater, toxicity  depends on  hardnessj nickel tends
to be more toxic in softer water.  Acute values for exposure
to a variety of nickel  salts* expressed a« nickel, range from
510 tig/liter for Daphnia magna to 46,200 ug/llter for banded
killifish at comparable hardness  levels.  Chronic values range
from 14.3 pg/liter for Oaphnia magna in  soft water to 530 pg/liter
for the fathead minnow  in hard water.  Acute-chronic  ratios
for Daphnia magna range from  14 in hard water to 83 in soft
water* and are approximately  50 in both  hard and soft water
for the fathead minnow.  Residue  data for the fathead minnow
indicate a bioconcentration factor of 61.  freshwater algae
experience reduced growth at  nickel concentrations as low as
100 ug/liter.

     Acute values for saltwater species  range from 152 ug/liter
for mysid shrimp to 350,000 pg/liter for the mummichog.  A
chronic value of 92.7 ug/littr is reported for the mysid shrimp,
which fives an acute-chronic  ratio of 5.5 for the species.
Reduced growth is seen  in saltwater algae at concentrations
as low as 1,000 (if/liter.  Bioconcentration factors ranging
from 299 to 416 have been reported for th« oyster and mussel.
Nickel
Page 3
October 1985
                                                  o«fn«*it AmaooatM

-------
 Regulations and  Standards

 Ambient Watt;  Quality Criteria  (DSEPA) t

     Aquatic Lift

     Freshwater

           Acute  tOBieltys   «t(K76  Hatb.rtWM)] * 4.02) M/llt-r

           Chronic  toaicitys  V°*7S  Jin(hardness)1 * l.Oi) Mg/liter

     Saltwater

           Acute  toiicityj   140  Mg/liter
           Chronic  toxicity:   7.1 yg/liter

     HumanHealth

     Criterion:  13.4 ug/litftr

 CAG Unit Rislc  (DSEPA):   1.15 (»g/kg/day) "l

 NIOSH Recommended  Standard:   15 Mi/a3 TWA (inorganic nickel)

 OSHA Standard;   1  ag/a  (a*tal and soluble conpounds/ as nickel)

 ACGIH Threshold  Liait. Values*

     0.1 ag/a? TWA (soluble  compounds, as nickel)
     0.3 ag/a  -STEL  (soluble coapoundsr as nickel)
     0.35  ag/a   TJfA  (nickel  car bony 1, as nickel)
     1 ag/a TWA (nickel  sulfide roasting, fuae and dust, as
       nickel; human  carcinogen)

 REFERENCES

 AMERICAN CONFERENCE OP GOVERNMENTAL INDOSTRIAL HYCIENISTS (ACGIH).
     1980.   Oocuaentation of  tbe Threshold Liait Values.  4th
     ed.   Cincinnati,  Ohio.   48S pages

NATIONAL ACADEMY 07 SCIENCES  (HAS).  1175.  Medical and Environ-
     mental  Effects of Invironaental Pollutants!  Nickel.
     Coaaittee on Medical and Biological Iffeets of Environmental
     Pollutants, Division of Medical Sciences, Rational Research
     Council, Washington, D.C.  277 pages
                        \
NATIONAL INSTITUTE FOR OCCUPATIONAL SAFETY AMD BEALTB (NIOSH).
     1977.   Criteria  for a Recoaaended Standard—occupational
     exposure to Inorganic Nickel.  Washington, D.C.  Nay 1977.
     DHEW  Publication No. (NIOSH) 77-164
Nickel
Page 4
October 1985

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 NATIONAL  INSTITUTE FOR OCCUPATIONAL SAFEU'i A«U
      1983.  Registry of Toxic Effects of Chemical  Substances.
      Data Base.  W»»hington, D.C.  October 1983

 5.S.  ENVIRONMENTAL PROTECTION AGENCY  (USSPA).  1979.  Water-
      Relatad Environaental fate of 129 Priority Pollutants.
      Washington, D.C.  December 1979.  EPA 440/4-79-029

 O.S.  ENVIRONMENTAL PROTECTION AGENCY  (DSEPA).  1980.  Ambient
      Water Quality Criteria for Nickel.  Office of Water Regu-
      lations and Standards, Criteria and Standards Division,
      Washington, D.C.  October 1910.  EPA 440/5-80-060

 U.S.  ENVIRONMENTAL PROTECTION AGENCY  (DSEPA).  1984.  Health
      Effects Assessment for Nickel.  Final Draft.  Environmental
      Criteria and Assessment Office* Cincinnati, Ohio.  September
      1984.  ECAOCIN-H01S

 O.S.  ENVIRONMENTAL PROTECTION AGENCY  (USEPA).  1985.  Health
      Assessment Document for Dichloroaethane  (Methylene Chloride).
      Office of Health and Environmental Assessment.  Washington,
      D.C.  February 1985.  EPA 500/3-32/004?

 WEAST, R.E.f ed.  1981.  Handbook of Chemistry and Physics.
      62nd ed.  CRC Press, Cleveland, Ohio.  2,332 pages
Nickel
Page S
October 1985

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                           NITROCELLULOSE
  Summary
       nitrocellulose with • largt percentage of the high-nitrogen
  fora is «xplo»iv«.


  Background Information

       nitrocellulose generally consists of a mixture of  high-
  nitrogen and low-nitrogen (pyroxylin)  forms of nitrated cellulose.
  The ratio of the tvo forms in a particular nitrocellulose con-
  pound varies,  nitrocellulose with a large amount of the high-
  nitrogen form is explosive ,  while nitrocellulose with mostly
  the low-nitrogen form is more stable.

  CAS Number:  9004-70-0

  Chemical Formula t   C-I-Q-CONO,)

  IUPAC Name;  Cellulose nitrate

  Important Synonyms  and Trade Names:   Cellulose tetranitrate,
                                       nitro cotton, soluble gun
                                       cotton r collodion

  Chemical and Physical Properties

  Molecular Weights   >504

  Boiling Point:   Explosive solid

  Melting Points   €?1*C

  Specific Gravltys   1.35-1.6

  Solubility in Wattes  insoluble

  Solubility in Organicsi  Soluble in ether and alcohol.

  flash Pointi 13*C


  Transport and Fata

       The limited information on the transport and fate  of nitro-
  cellulose indicates that it  emits high levels of nitrate and
  nitrite when present in a landfill.   This suggests that nitro-
  cellulose may eventually degrade to cellulose or at least to
  fairly stable low-nitrogen nitrocellulose.  After prolonged
  storage, nitrocellulose plastics emit camphor.  This decay

  Nitrocellulose
  Page 1
  October IfiS
Preceding page blank

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 can decrease decomposition  temperature and thus ipeed up decom-
 position, probably with the formation of nitrates and nitrites.


 Health Iffeets

     According  to the extremely limited information on the
 toxicity of nitrocellulose, it is not very toxic.  Its explosive
 tendency would  be the primary concern associated with exposure
 to nitrocellulose at a waste site.


 Toxicity to Wildlife and Peaestie Aniaals

     Ho information on the  toxicity of nitrocellulose to wildlife
 and domestic animals was found in the sources reviewed.


 Segulations and Standards ..=

     Ho regulations or standards based on the toxicity of nitro-
 cellulose have  been established.
REFERENCES

TEE CONDENSED CHEMICAL DICTIONARY.  1977.  9th ed.  G.G. Hawley,
     ed.  Van Nostrand Reinhold Co., Hew Tors

KIRK-OTHMEH ZHCYCLOPEDIA OF CHEMICAL TECHNOLOGY.  1979.  3rd
     ed.  Vol. 5:  Castor Oil to Chlorosulfuric Acid.  John
     Wiley and Sons, Hew York

THE MERCK INDEX.  1976.  9th ed.  Windholi, M., ed.  Merck
     and Co., Rahway, New Jersey

NATIONAL INSTITUTE FOR OCCUPATIONAL SAFETY AND HEALTH  (NIOSI).
     1984.  Registry of Toxic Effects of Chemical Substances.
     Data Base.  Washington, D.C.  October 1984

TOXICOLOGY DATA BANK (TDB).  1985.  The online toxicology data
     bank of the national Library of Medicine (HLM):  Collodion.
     NLM, Bethesda, Maryland.  January 1985

WEAST, R.E., ed.  1981.  Handbook of Chealstry and Physics.
     62nd ed.  OtC Press, Cleveland, Ohio.  2,332 pages
Nitrocellulose
Page 2
October 1985

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                           HITROPHENOL
 Summary
     Nitrophenol  is reported to cause liver and kidney daaage
 in experimental animals,  it aay have a direct effect on cell
 membranes  in general.
 CAS Numbert  2-nitrophenol:  88-75-5
             3-nitrophenol:  554-84-7
             4-nitrophenol:  100-02-7
 Chemical Formulas  CgH02H4OH
 ID?AC Name:  o-,  a-f oe p-Nitrophenol
 Important  Synonyms and Trade Names:  Nitrophenol, hydroxy-
                                     nitrobentene, aononitrophenol
Chemical and Physical Properties
Molecular weight:  139.11
Boiling Point:  2-nitrophenol:  216»C
                3- and 4-nitrophenol:  279*C
Melting Pointx  2-nitrophenol:  45.3*C
                3-nitrophenol:  S7*C
                4-nitrophenol!  113-c
Specific Gravity:  l.S at 20*C
Solubility in Wateri  2,100 mg/liter at 20*C
Solubility in Organics:  Soluble in alcohol, ether, acetone*
                         benzene, and chloroform
Log Oct and/Water Partition Coefficient!  1.76
Vapor Pressure:   1 aa eg at 50*C
pKa:  7.2

Transport and Pate
     Based on inforaation concerning 4-nitrophenol, it appears
that photoozidation of the nitrophenols to catechol and nitrohy-
droquinone is their priaary degradative pathway.  There is,

Mitrophenol
Page 1
October 1915

-------
 however*  a  possibility  that  organic Material to which nitrophcnol
 becomes adsorbed say  act  aa  a  reducing agent in the photoreduc-
 tion of this compound to  aminophenol and dlhydroxyazobenzene.
 Oxidation by hydroxyl radicals aay also occur,  consideration
 of  the low  vapor pressure, relative high solubility in water,
 and moderate lonizatlon constant of nitrophenol auggeats that
 volatilisation  is  not an  important transport process.  Although
 aorption  of nitrophenol by organic materials probably occurs
 to  only a limited  extent, it appears that stable complexes
 with clay mineral  and soils  can be formed.  Furthermore, there
 is  a small  possibility  that  nitrophenol can undergo hydrolysis
 within the  clay structure.

     Bloaccumulation  and  biomagnification do not appear to
 be  important processes  for nitrophenol.  Biotransforaation
 processes,  including  reduction of the nitro group, hydroxylation
 of  the aromatic ring, and displacement of the nitro group by
 a hydroxy group, can  be demonstrated with soil or water micror-
 ganisas under optimal conditions.  Some studies suggest that
 nitrophenol is  very persistent in aqueous soil cultures and
 can Inhibit microbial growth in natural aquatic systems through
 its action  as an oxidative phosphorylation uncoupler.  However,
 results of  other studies  suggest tbat it is readily and rapidly
 degraded, especially  by acclimated microorganism populations.


 Health Effects

     Based  on the  results of limited testing, nitrophenol does
 not appear  to pose carcinogenic or mutagenic haxards (USEPA 1980}.
 4-Hitrophenol is currently being tested for carcinogenic!ty
 by  the national Toxicology Program.  No data concerning teratogenic
 potential are available.

     Very little information concerning the toxicity of nitro-
 phenol Is available.  This coapound Is reported to cause kidney
 and liver injury in experimental animals.  Administration of
 10  ag of  4-nitrophenol, 30 mg  of 3-nitrophenol or 100 mg of
 2-nitrophenol by gavage to anesthetized rats Is reported to
 significantly Increase  respiratory volume.  Hitrophenol can
 inhibit chlorine transport in  red blood cells, suggesting a
 direct effect on cell membranes*

     A significant increase  in blood platelet levels was observed
 in  rats after intraperitoneal  injection of as little as 0.1 ag/kg
of  2-nitrophenol.  This effect was not seen when the other
nltrophenols were administered.  Oral LD*n values of 620 tag/kg
for 4-nitrophenol, 930 ag/kg for 3-nitropnenol and 2,828 ag/kg
for 2-nitrophenol are reported for the rat.
Hitrophenol
Page 2
October 1985

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   Toxlcity to Wildlife and Doaestie Animals
        i«r«i^«a 24-hour LCSQ values range from 35,000 Mg/liter
   for 4-nitrophenol to 2107000 pg/liter for 2-nitrophenol for
   the freshwater species Oaphnia nagna and frcn 8,000 (4-nitrophenol)
   to 67,000 (2-nitrophenol)  pg/liter tor the bluegill.   A concentra-
   tion of 33,300 pg/liter of 2-nitrophenol caused  381 mortality
   in goldfish in eight hours*  96-Hour lethal threshold  values
   of 26,000 (4-nitrophenol)  and 32,900 pg/liter 2-nitrophenol
   are reported {or the saltwater shrimp, Crangon septeasptnosa.

        A nitrophenol concentration of 35,000 pg/liter inhibits
   chlorophyll synthesis after 3 days in the freshwater alga,
   Chlorella pyrenoidosa.  Growth of duckweed is reduced  501 by
   a concentration of £2,550  tig/liter of 2-nitrophenol.

        The weighted average  bioeoncentration factor  for  the edible
   portion of all freshwater  and estuarine aquatic  organisms con-
   sumed by Americans is 2.33.


   Regulations and Standards

   Aabient Water Quality Criteria (DSEPA)i

        The available data are not adequate for establishing criteria.


   REFERENCES

   NATIONAL INSTITUTE FOR OCCUPATIONAL SA7ETY AND HEALTH  (NIOSH).
        1984.   Registry of Toxic Effects of Chemical  Substances.
        Data Base.   Washington, D.C.  January 1984

.-•   SAX,  N.I.   1975.   Dangerous Properties of Industrial Materials.
        4th ed.   Van Hostrand Reinhold Co., Hew fork.  1,258 pages

   D.S.  ENVIRONMENTAL PROTECTION AGENCY (USEPA). 1979.   Water-
        Related  Environmental Fate of 129 Priority  Pollutants.
        Washington,  D.C.  December 1979.  EPA 440/4-79-029

   O.S.  ENVIRONMENTAL PROTECTION AGENCY (DSEPA). 1980.   Ambient
        water  Quality Criteria for Nitrophenols. Office  of Water
        Regulations  and Standards, Criteria and Standards Division,
        Washington,  D.C.  October 1980.  SPA 440/5-80-063

   WZAST,  R.8.,  ed.   1981.  vHandbook of Chemistry and  Physics.
        62nd  ed.   CRC Press,  Cleveland, Ohio.   2332 pages
  Witrophenol
  Page 3
  October 1985
                                                    [Ciemanc Ammocmomm

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                         PENTACHLOROPHENOL
 Summary

     Pentachlorophenol  in  probably persistent  in  natural  environ-
 ments.   It  is embrydtoxic  and  fetotoxic.  Chronic exposure
 has  been shown  to  cause chloracne, headache, muscle weakness,
 weight loss, and liver  and kidney damage.  Technical  grade
 pentachlorophenol  is often contaminated with polychlorinated
 dibenzo-p-dioxins,  and  these contaminants nay  be  responsible
 for«*sbme of the toxic effects  associated with  exposure  to penta-
 chlorophenol.   Pentachlorophenol is highly toxic  to aquatic
 organisms.
CIS Numbert   87-86-5

Chemical Formulas  CgCl^OH

IUPAC name:   2,3,4,5,6-Pentachlorophenol

Important Synonyms and Trade namess  PC?,  DP-2  antimicrobial,
                                     Dowieide 7,  Duroto*.


Chemical and  Physical Properties

Molecular weights  266.32

Boiling Points  Decomposes  at  309*C

Melting Point!  199~191*C

Specific Gravitys  1.978 at 20*C

Solubility in Water*  14 mg/liter  at 20»C»  the  sodium  salt
                    . of pentachlorophanate is  highly  soluble
                      In water

Solubility in Organic*s  Very  soluble  in alcohol  and etherj
                         soluble  in hot benzenei  slightly soluble
                         in ligroin and other solvents
Log Octanol/Water  Partition Coefficients   5.01

Vapor Presi

pXai  4.74
Vapor Pressures  1*1 x 10*  ma Eg at  20*C
Pentachlorophenol
Page  1
October  1983
                                               ^Jciaffwic Ammocimtmm

Preceding page blank

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Transport and Pat*

     There i» little infornatlon on the transport of pentachloro-
phenol through the environment.  The compound has a low vapor
pressure and, therefore, is not likely to volatilize readily.
It is slightly soluble in water and does adsorb to sediments,
and therefore may be transported through toil, surface water,
and groundwater.

  ..• fentaehlorophenol is degraded by sunlight to lower chlorin-
ated*'phenols., tetraehlorodihydroxyl benzenes, and non-aromatic
fragments*  The importance of photodegradation of pentachloro-
phenol in the environment is unknown.  Soil microorganisms
have also been found to degrade pentachlorophenol.  However,
the compound was persistent in sediments and leaf litter follow-
ing a spill into a freshwater lake.  Limited information on
bioconcentration of pentachlorophenol in freshwater species
suggest a bioconcentration factor of 500; in saltwater species
factors vary from 13 to 3,830.  Some pentachlorophenol residues
found in tissue may actually be the result of metabolism of
hexaehlorobenzene.


Health Effects

     Fentaehlorophenol has not been found to be nutagenic or
carcinogenic in the studies reviewed,  ft is currently under
study by the National Toxicology Program for its carcinogenic
potential.  No teratogenlc effects have been reported in the
studies reviewed, but pentachlorophenol has been shown to be
embryotoxic and fetotoxic.  Fentaehlorophenol has not been
found to be highly toxic upon chronic exposure, although fatal
cases from acute and chronic human exposures have been reported.
Chloracne is the major effect associated with human chronic
exposures, however, this may actually be caused by the polychlori-
nated dibenzo-dioxin contaminants found in technical grade
pentachlorophenol*  Other effects associated with chronic intoxi-
cation include muscle weakness, headache, anorexia, abdominal
pain, weight loss, and effects on the liver and kidneys.  Effects
on the liver and kidney were less severe in animals treated
with purified pentachlorophenol compared to technical grade
compound.


Toxieity to Wildlife and Domestic animals

     Concentrations ranging from 34 to 2,000 ug/liter have
been found to be acutely toxic to freshwater aquatic organisms.
Toxieity is greater at acidic pH values than alkaline pH values.
Growth of salmonid fish species is affected by pentachlorophenol
at even lower concentrations.  Some freshwater aquatic plants
have also been shown to be sensitive to the compound but this
has not been studied in detail.


Pentachlorophenol
Page 2
OotOb.. IMS

-------
 Regulations  and  Standards

 Aabient Water  Quality Crittria  (USEPA)z

      Aquatic Life

      The available data  are not  adequate foe establishing criteria.

      Human Health

      Health  criterion!   1.01 mg/liter
      Orfanoleptic criterions  30 Mi/liter

 OSHA  Standard:   500  pg/a3 TWA

 ACG1H Threshold  Limit values:  O.S ag/m3,
O.S mg/m; TWA
i.s ag/mj STB;
                                         STEL
 REFERENCES
AMERICAN CONFERENCE OF GOVERNMENTAL INDUSTRIAL HYGIENISTS  (ACGIH).
     1980.  Documentation of the Threshold Limit Values.   4th
     ed.  Cincinnati, Ohio.  488 pages

NATIONAL INSTITUTE FOR OCCUPATIONAL SAFETY AND HEALTH  (NIOSH).
     1983.  Registry of Toxic Effects* of Chemical Substances.
     Data Base.  Cincinnati, Ohio.  October 1983

RAO, K.R., ed.  1978.  Pentachlorophenolj  Chemistry, Pharmacology,
     and Environmental Toxicology.  Environmental Science  Research
     volume 12.  Plenum Press, New fork

U.S. ENVIRONMENTAL PROTECTION AGENCY OJS2PA}.  1979.  Water-
     Related Environmental Fate of 129 Priority Pollutants.
     Vol. 2.  Washington, D.C.  December 1979.  EPA 440/4-79-029

U.S. ENVIRONMENTAL PROTECTION AGENCY (USEPA).  1980.  Aabient
     Water Quality Criteria for Pentachlorophenol.  Office
     of Water Regulations and Standards, Criteria and Standards
     Division, Washington, D.C.  October 1980.  EPA 440/5-80-065

O.S. ENVIRONMENTAL PROTECTION AGENCY (USEPA).  1984.  Health
     Effacts Assessaent for Pentachlorophenol.  Environmental
     Criteria and Assessment'Office, Cincinnati, Ohio.   September
     1984.  ECAO-CIN-H043  (Final Draft}

WEAST, R.E., ed.  1981.  Handbook of Chemistry and Physics.
     62nd ed.  CRC Press, Cleveland, Ohio.  2,332 pages
Pentachlorophenol
page 3
October 1985

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                            PREKANTHRENE


  Suncnary

       Phenanthrene is a polycyclic  aromatic hydrocarbon  (PAR)
  and is moderately persistent in  natural  environments,   In  two
  •kin painting studies, it produced appli cat ion- site tumors,
  and it was shown to be mutagenic in several other studies.
  Workers exposed to materials containing  phenanthrene developed
  chronic dermatitis and other skin  disorders.


  CAS Nunberj   35-01-8

  Chemical Poraulas  ci4Hio

  IUPAC (fame:   Phenanthrene


  Chemical and  Physical Properties

  Molecular Height:  171.24

  Boiling Point:   34G*C

  Melting points   101»C

  Specific Gravltyt  1.025

  Solubility in Water:  1.29 mg/liter at 25*C

  Solubility in Organicsi   Soluble in alcohol,  ether, acetone,
                           benzene,  and acetic  acid

  Log Octanol/Water Partition  Coefficients 4.46

  Vapor Pressure!  6.9 x 10   am Hg  at 20 *C

  Vapor Density i   C.14


  Transport and Fate

       Much of  the Information concerning  transport and fate
  is  inferred Iron data for polycyclic aromatic hydrocarbons
  (PAfls)  in general because specific information for phenanthrene
  is  lacking.   Rapid, direct photolysis of phenanthrene to quinones
  •ay occur in  aqueous solution.  Oxidation is  probably too  slow
  to  be a significant environmental  process and the available
  data suggest  that volatilisation generally is not an important
  transport process.  The calculated log octanol/water partition


  Phenanthrene
  ?«§« 1
  October 1185
Preceding page blank

-------
coefficient of  4.46 indicates that the compound should be strongly
absorbed onto participate Batter, especially particulars high in
organic content.   It  is likely that phenanthrene can be trans-
ported as absorbed matter on suspended partieulates in air
or water.  Data for PAHs in general indicate that phenanthrene
vill accumulate In the sediment and biota of the aquatic environ-
aent.  Removal  rates  associated with absorption and subsequent
sedinentation are  probably slower than photolysis and degradation,
but aay be competitive with volatilization.

     Data for a variety of PAHs suggest that bioaccumulation is
a short tern process, and long-term partitioning into biota is
not a significant  fate process.  Phenanthrene can be metabolized
by multicellular organlsas and degraded by aierobes.

     Degradation by mammals is likely to be incomplete, with
parent compound and the metabolites being excreted by the urinary
system.  Biodegradation by microorganisms Is probably the ulti-
mate fate process.  Biodegradation generally appears to be more
efficient In soil  than in aquatic systems*  However, it may be
more important  in  those aquatic systeas which are chronically
affected by FAB contamination,  phenanthrene is stable enough
in air to be transported over relatively great distances.


Health Effects

     There are  no  epideaiologlcal or ease studies available
suggesting that phenanthrene is carcinogenic in huaans.  This
compound generally is not considered to be carcinogenic in
experiaental aniaals.  However, at least two skin painting
studies report  development of tumors at the site of application
in alee.  Phenanthrene exhibits mutagenic activity in soae test
systems, but not in others.  There are no reports of teratogenic
or reproductive effects due to phenanthrene exposure.

     Little information concerning acute and chronic toxic
effects is available.  Although specific data concerning exposure
to phenanthrene are not available, workers exposed to aaterials
containing this compound aay exhibit chronic deraatitis, hyper*
keratoses, and  other skin disorders.


Toxiclty to Wildlife and Domestic Aniaals

     Adequate data for characterization of toiiclty to doaestic
aniaals and wildlife ace not available*  A 96-hour LC5Q value of
COO pg/liter is reported for a saltwater polyehaete wofa exposed
to • crude oil  fraction containing phenanthrene.  The weighted
average bioconcentration factor for the edible portion of all
freshwater and  estuarlne aquatic organisas consuaed by Aaerleans
is 486.


Phenanthrene
Page 2
October 198S

-------
    Regulations and Standards

I    Ambient Watte Quality Criteria  (USEPA):

         Aquatic Life

         The available data are not  adequate  for establishing criteria.

         Human Health

         Estimates of the carcinogenic  risks  associated with lifetime
         exposure to various concentrations of  carcinogenic PAHs
         in water are:


         Risk                        Concentration

         10"e                        28 ng/liter
         10",                        2.8 ng/liter
         10"7                        0.28 ng/liter



    REFERENCES

    NATIONAL INSTIDTE FOR OCCUPATIONAL  SAFETY AND HEALTH  (NIOSH).
         1984.  Registry of Toxic Effects of  Chemical Substances.
         Data Base.  Washington, D.C.  April  1984

    SANTODONATO,  J.,  HOWARD, P., and BASD, D.   1981.  Health and
         ecological assessment  of polynuclear aromatic hydrocarbons.
         J.  Environ,  fatb. and  Toxicol.  5:1-364

    SAX,  N.I.   1975.   Dangerous Froperties of Industrial Materials.
         4th ed.   Van Nostrand  Relnhold Co.*  New York.  1,258 pages

    U.S.  ENVIRONMENTAL PROTECTION AGENCY (DSEPA).   1979.  Water-
         Related Environmental  Fate  of  129 Priority Pollutants.
         Washington,  D.C.  December  1979. EPA  440/4-79-029

    0.5.  ENVIRONMENTAL PROTECTION AGENCY (DSEPA).   1980.  Ambient
         Water Quality Criteria for  Polynuclear Aromatic Hydrocar-
         bons*.  Offlc* of Water Regulations and Standards, Criteria
         and Standards Division, Washington,  D.C.   October 1980.
         EPA 440/5-80-069

    D.S.  ENVIRONMENTAL PROTECTION AGENCY (DSEPA).   1984.  Health
         Effects Assessment for Phenanthrene.   Environmental Criteria
         and Assessment Office,  Cincinnati, Ohio.   September 1984.
         ECAO-CIN-H029  (Final  Draft}

    WEAST,  R.E.,  ed.   1981.  Handbook of Chemistry  and Physics.
         62nd ed.  CRC Press, Cleveland, Ohio.  2332 pages

    Phenanthrene
    Page  3
    October  1965

-------
 Regulations and Standards

 Ambient Water  Quality Criteria  (DSEPA)t

      Aouatic Life

      The available data  are  not  adequate  for establishing criteria,

      Human Health

      Estimates of  the carcinogenic risks  associated with lifetime
      exposure  to various concentrations of carcinogenic PAHs
      in water  are:


      R i sk                       Concentration

      ID"*                       28 ng/llter
      10"l                       2.8 nf/liter
      10                         0.28 ng/liter



 REFERENCES

 NATIONAL INSTIUTE  FOR OCCUPATIONAL SAFETY AND HEALTH  (NIOSH).
      1984.   Registry  of  Toxic Effects of  Chemical Substances.
      Data Ease.  Washington, D.C.  April  1984

 SANTODONATO, J., HOWARD, P., and BASO, D.  1981.  Health and
      ecological  assessment of polynuclear aromatic hydrocarbons.
      J.  Environ. Path, and Toxicol. 5:1-364

 SAX,  N.I.   1975.   Dangerous Properties of Industrial Materials.
      4th ed.  Van  Nostrand Reinhold Co.,  New York.  1,258 pages

 O.S.  ENVIRONMENTAL PROTECTION AGENCY (OSEPA).  1979.  Water-
      Related Environmental Fate of 129 Priority Pollutants.
      Washington, D.C.  December 1979.  EPA 440/4-79-029

 O.S.  ENVIRONMENTAL PROTECTION AGENCY (DSEPA).  1980.  Ambient
      Water  Quality Criteria for Polynuclear Aromatic Hydrocar-
      bons*  Office  of Water Regulations and Standards, Criteria
      and Standards Division, Washington,  D.C.  October 1980.
      EPA 440/5-60-069

 O.S.  ENVIRONMENTAL PROTECTION AGENCY (OSEPA).  1984.  Health
      Effects Assessment  for Phenanthrene.  Environmental Criteria
      and Assessment Office, Cincinnati, Ohio.   September 1984.
      ECAO-CIN-H029  (Final Draft)

WEAST, R.S., ed.   1981.  Handbook of Chemistry and Physics.
      82nd ed.  CRC  Press, Cleveland, Ohio.  2332 pages

 Phenanthrene
 Page  3
 October  1985                                   m
                                               ^Tciemanc Ammo

-------
                              PHENOL
 Summary
     When applied to the skin of mice, phenol appears to have
 some tumor-promoting effects and nay b« a weak carcinogen.
 There  is equivocal evidence that phenol is autagenic.  Subchronic
 exposure to phenol caused liver, kidney/ lung, and heart damage
 in  experimental animals,  in humans, phenol has been shown
 to  irritate the eyes, nose, and throat*  •
CAS Number i  108-95-2
Chemical Formula j  CgBgOB
I UP AC Name:  Phenol
Chemical and Physical Properties
Molecular Weights  94.11
Boiling Pointi' 181.7S*C
Melting Point i  43 *C
Specific Gravity!  1.0576 at 20*C
solubility in Water i  93,000 mg/liter at 25 *C
                                    *
Solubility in Organics:  Soluble in alcohol, chloroform, and
                         carbon disulfidej very soluble in ether;
                         miscible with carbon tetrachloride
                             hot benzene
Log Octanol/Water Partition Coefficient:  1.46
Vapor Pressurei  0.3513 mm ig at 2S*C
Vapor Density t  3.24
pKai  10.02
Flash Point t  85 «C  {closed cup)
Phenol
Page 1
October 1985

-------
      photooxidation may be an Important degradative process,
 especially  in  aerated, clear, surface waters.  Phenol nay also
 be  nonphotolytically oxidized in highly aerated waters that
 contain  iron and copper in solution or as part of the suspended
 particulates.  The relatively low log octanol/water partition
 coefficient of phenol, as well as the available experimental
 evidence, suggest that sorptlon and bioaccumulation are not
 important environmental fate processes.  Biodegradation can
 be--a  significant fate pathway in aquatic systems and soil when
 significant -concentrations of microorganisms are present.
 In 'addition to microorganisms, at least one species of fish
 is  reported to be able to biotransform phenol.

      The dominance of photooxidation, metal-catalyzed oxidation,
 or  blodegradatlon as destructive pathways depends on the partic-
 ular  environmental conditions, but the degradation products
 are similar for all fate pathways.  The first step usually
 involves further hydroxylation of the aromatic ring, followed
 by oxidation to benzoquinone and cleavage of the ring structure.
 There is a  possibility that phenol present in surface waters
 can volatilize into the atmosphere.  However, since this phenol
 would be rapidly photooxidized in the troposphere* any signifi-
 cant  atmospheric transport is unlikely.


 Health iffects

      Phenol appears to have tumor-promoting activity in many
 strains of  mice when repeatedly applied to the shaved skin
 after initiation with known carcinogens,  although there is
 equivocal evidence that phenol may be weakly carcinogenic when
 applied to  the skin of one sensitive strain of mice, it does
 not appear  to be carcinogenic when applied to the skin of stan-
 dard  strains of mice.  NCI reported that phenol was not carcin-
 ogenic when administered in drinking water to rats and mice.
 There is equivocal evidence that phenol may have mutagenic
 effects, although further evaluation is needed.  There are
 no reports  of  teratogenie effects caused by exposure to phenol.

      Subchronic inhalation exposure to phenol is reported to
 cause liver, kidney, lung, and heart damage in guinea pigs.
 Slight liver and kidney damage was seen in rats exposed by
gavage to 100 mg/kg/day for 20 days.  The oral and skin IB..S
 for the rat art 414 aad 669 mg/kg, respectively, and the innala-
 tion LC«Q is 316 mg/m . ^Phenol is an eye, nose, and throat
 irritant and can cause systemic damage to the nervous system
 in humans following dermal, oral, or inhalation exposure.
Phenol
Page 2
October 1985

-------
 Toxieitv  to Wildlife and Domestic Animals

     The  acute toxicity of phenol to freshwater species  is
 expressed over m  range of 2 to  3 orders of magnitude.  Acute
 values for fish species range from  5,020 tig/liter for juvenile
 rainbow trout to  67,500 ug/liter for the fathead minnow.  The
 •cutt value for the rainbow trout,  and a value of 5,000  jig/liter
 for Oaphnta aagna art the lowest acute values observed.  An
 early lite stage  test on the fathead minnow resulted in a chronic
 value of  2,560 ug/liter* with an acute-chronic ratio of  14.
 Median effect concentrations for oyster and clan embryos are
 approximately 55,000 ug/liter.  For the grass shrimp and the
 mountain  bass, LC«g values of 5,800 and 11,000 ug/liter, respec-
 tively, are reported.  No chronic effects are available  for
 saltwater species.  Reported bioeoncentration factors of 1.2
 to 2.3 for goldfish suggest that no residue problem should
 occur froa exposure to phenol.  Ho appropriate data concerning
 effects of phenol on other wildlife or domestic animals are
 available.


 Regulations and Standards

Aabient Water Quality Criteria  (OSEPA)t

     Aquatic Life

     The  available data are not adequate for establishing criteria,
     However, the lowest concentrations of phenol known to
     cause toiie effects in aquatic organisms ares

     Freshwater

       Acute toxicity:  10,200 ug/liter
       Chronic toxicity:  2,560 ug/liter

     Saltwater

       Acute toxicityi  5,800 Mg/liter
       Chronic toxicity:  Ho available data

     Human Health

     Health criterion:  3.5 us/liter
     Organoleptic criterion:  0.3 mg/liter

                      x

NIOSH Recommended Standards:  20 ag/a, TWA
                              60 ag/nvlS ain Ceiling Level

OSHA Standard:  19 ag/a3
Phenol
Page 3
October 1985

-------
 .......  ....	.-•-  *«*»i*i.  **t
                                38 mg/wT  STEL

 Department  off Transportations   poison


 REFERENCES

 AMERICAN CONFERENCE OP GOVERNMENTAL  INDUSTRIAL 1YSIBNISTS  (ACGIH)
     1980.  Documentation  of the Threshold Liait Values.   4th
     *d.  Cincinnatir  Ohio.  488 pages

 NATIONAL CANCER  INSTITUTE  (NCI).  1980.  Bioassay of Phenol
     foe Possible Caretnogenieity.   CAS  No. 108-95-2.  NCI
     Carcinogenesis Technical Report Series No. 203.  Washington,
     B.C.   DSOHHS Publication No.  (NTP)  80-15

 NATIONAL INSTITUTE FOR OCCUPATIONAL  SAFETY AND HEALTH  (NIOSH).
     1983.  Registry of Toxic Effects of Chemical Substances.
     Data Base.  Washington, D.C.  October 1983

 SAX, N.I.   1975.  Dangerous Properties of Industrial Materials.
     4th ed.  Van Nostrand Reinhold  Co., New York.  1,258  pages

 U.S. ENVIRONMENTAL PROTECTION AGENCY (US.EPA).  1979.  Water-
     Related Environmental Fate of 129 Priority Pollutants.
     Washington, D.C.  December 1979.  EPA 440/4-79-029

U.S. ENVIRONMENTAL PROTECTION A6EMCT (DSEPA).  1980.  Aabient
     water  Quality Criteria for Phenol.  Office of Water Regu-
     lations and Standards, Criteria and Standards Division,
     Washington, D'.C.  October  1980.  EPA 440/5-80-066

U.S. ENVIRONMENTAL PROTECTION AGENCY (USEPA).  1984.  Health
     Effects Assessaent for Phenol*  Environmental Criteria
     and Assessaent Office, Cincinnati,  Ohio.   September  1984.
     ECAO-CIN-H007   (Final Draft)

WEA5T, R.S., ed.  1981.  Handbook of Chemistry and Physics.
     62nd ed.  CRC Press, Cleveland, Ohio.  2,332 pages
Phenol
Page 4
October 1985

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                           PHENYL  ETHER
Summary
     Phenyl tther it somewhat persistent In the natural envi-
ronment.  It can cause nausea in humans.  High concentrations
of phenyl ether irritate the akin.


CAS Number:  101-84-8

Chemical Foraulas  CfiHe-O-CsHs

IUPAC Name:  Phenoxybenzene

Important Synonyms and Trade Names:  Diphenyl ether, diphenyloxide,
                                     phenoxyben zene


Chemical and Physical Properties

Molecular Weight:  170.20

Boiling Point?  257-25S*C

Melting Points  2S*C

Specific Gravity:  1.073 it 20«C

Solubility in Water:  Insoluble in water

Solubility in Organics:  Soluble in alcohol, benzene, ether,
                         and glacial acetic acid

Log Octanol/Water partition Coefficient;  4.1 (calculated)

Vapor Pressure;  0.02 mm, Ig at 25*C

Vapor Density:  5.86

Flash Points  115*C


Transport and Pate
                        v
     No information on the transport and fate of phenyl ether
was found in the literature reviewed, but information was avail-
able on 4-chlorophenyl phenyl ether.  Based on this information
and on the chemical and physical properties of phenyl ether,
probable transport and fate processes can be determined.
Phenyl ether
Page 1
October IfiS
                          133

-------
      Although  phenyl  ether  has  a  low  vapor pressure,  its  low
 water solubility  suggests that  United  volatilization is  likely.
 Once in the  atmosphere,  it  will be photooxidized.   Phenyl ether
 has  a high log octanol/water partition  coefficient} it probably
 both adsorbs to soil  and sediments and  bioaccuaulatts.  The
 results of a study on 4-chlorophenyl  phenyl ether suggest that
 biodegradation nay be important in acclimated aierobial popu-
 lations but  not in populations  in natural waters.   Phenyl ether
 is likely to be somewhat persistent in  the natural  environment,
 with adsorption to organics acting as a storage mechanism.


 Health  Effects

      Phenyl  ether has not been  reported to be carcinogenic,
 nutagenic, or  teratogenic.  A disagreeable odor and possible
 nausea  provide.sufficient warning of  exposure.  The undiluted
 material  is  somewhat  irritating to the  skin after prolonged
 exposure, and  erythema and  exfoliation  are possible.  However,
 the  irritation clears promptly  once exposure ceases*  The oral
 L0-n for  rats  is  3.99 g/fcg; for the guinea pig, it  is approx-
 inliely 2.5  g/kg.


 Toxicitv  to  Wildlife  and Domestic Animals

      The  96-hour LC-0 values for phenyl ether are 9.6 ag/liter
 for  the fathead ainflow and  0.72 mg/liter for Daphnia nagna.


 Regulations  and Standards

 OSHA standard  (iir)s   7  mg/m3 TWA

 ACGIH Threshold Limit Values:   7 ag/a3-TN&
                                14 mg/mj S.TEL


 REFERENCES

 AMERICAN CONFERENCE OF GOVERNMENTAL INDUSTRIAL HYGIEN1STS (ACGIH)
      1980.   Documentation of the Threshold Limit Values.  4th
     •d.  Cincinnatir  Ohio.  4SS pages

 LYMAN,  W.J., R2EHL, W.r/, and ROSENBLATT, D.E.  1912.  Handbook
     of Chemical property Estimation  Methods?  Environmental
     Behavior  of Organic Compounds.   McGraw-Hill Book Co.,
     New York

 THE MERCK INDEX.  1976.  9tb ed,  Windholi, M., ed.  Merck
     and Co.,  Rahway,  Rew Jersey
Pbenyl ether
Page 2
October 1985

-------
 NATIONAL  INSTITUTE FOR OCCUPATIONAL SAFETY AND IEALTB  (NIOSH),
      1984.  Registry of Toxic Effects of Chemical Substances.
      Data Base.  Washington, D.C.  October 1984

 SAX,  N.I. 1975.  Dangerous Properties of Industrial Materials.
      4th  ed.  van Jiostrand Reinhold Co., New York*  1,258 pages

 D.S.  ENVIRONMENTAL PROTECTION AGENCY  (OSEPAJ.  1979.  Hater-
      Related Environmental Pate of 129 Priority Pollutants.
      Washington, D.C.  December 1979.  SPA 440/4-79-029

 VERSCHUEREN, K.  1977.  Handbook of Environmental Data on Organic
      Chemicals.  Van Nostrand Reinhold Co., Nev York.  659 pages

 WEAST» R.E., ed.  1981.  Handbook of Chemistry and Physics.
      62nd ed.  CRC Press, Cleveland, Ohio.  2,332 pages
phenyl ether
Page 3
October 1985
                                                 [Cl*m«nt Ammocmtmm

-------

-------
                           PHOSPHORIC ACID
  Summary
       Solutions of phosphoric acid act corrosive and are severely
  irritating to the sfcin, eyes, and mucous membranes.
  CAS Humbers   7664-38-2
  Chemical Formula:  H3P04
  IUPAC Name:   Phosphoric acid
  Important Synonyms and Trade Names:   Orthophosphoric acid

  Chemical and Physical Properties
  Molecular Weight:  98.04
  Boiling Point:  Loses one-half HjO at 213*C
  Melting Point:  42.35«C
  Specific Gravity:  1.834 at 18*C
  Solubility in Water:  Soluble in water
  Solubility in Organics:  Soluble in alcohol
  Log Octanol/Water Partition Coefficient:  -1.6 (calculated)
  Vapor Pressure:   0.0285 BID Hg at 20*C
  Tribasic acids  pl^-2, pk2-7' P^-i*
  Transport and Pate-
       Ho information on the transport and fate of phosphoric
  acid was found in the literature reviewed.  Phosphoric acid
  probably is  not very volatile.  It is soluble in water, and
  the degree of solubility depends on the pB of the water.  It
  •ay form insoluble salts and precipitate in association with
  such metals  as iron, aluminumf and zinc.  Its movement through
  soils is dependent on their pfi and may be limited by binding
  to minerals.
  Phosphoric acid
  Page 1
  October 1985
Preceding page blank

-------
 Health  Effects

      Phosphoric  acid, 13PO4»  ii  a  tribaaic acid  in which  the
 first hydrogen is  strongly  ionizing, the  second  moderately
 ionizing,  and the  third  very  weakly ionizing.  Solutions  of
 trihydrogen  phosphate are acidic and corrosive.  Phosphoric
 acid  is stronger than acetic  acid  but weaker than hydrochloric,
 nitric, or sulfuric  acid.   Phosphoric acid is a  severe irritant
 to skin, MUCOUS  membranes,  and eyes; and  the level of irritation
 is positively correlated with the  degree  of acidity.  Phosphoric
 acid  has no  known  carcinogenic,  mutagenic, or teratogenic prop-
 erties.  The oral  LD,n for  rats  is 1,530  ag/kg,  while the dermal
 LD50  for rabbits is  17740 ag/kg.


 Toxicity to  Wildlife and Domestic  Animals

      The toxicity  of phosphoric  acid to aquatic  organisms is
 due to  its acidic  nature, and therefore the toxic concentration
 will  depend  upon the buffering capacity of the natural waters,
 as well as the relative  resistance of each organism to low
 pB conditions.   Phosphoric  acid  nay be most harmful to the
 environment  because  it is an  important nutrient  and not because
 of its  toxieity.   Phosphate is very often the nutrient that
 by its  absence limits the growth of algae,  in the presence
 of sufficient phosphate, algal blooas occur which, as they
 die and  decay, lead  to eutrophication of  the body of water
 and cause  the elimination of  species that need higher oxygen
 levels  and a aor*  pristine  environment.   Airborne phosphoric
 acid  should  not  cause necrosis of  vegetation or  irritation
 to domestic  animals  at concentrations below 1 «g/m , but  such
 effects  are  possible at  higher concentrations.   Phosphoric
 acid  does  not bioaecuaulate in the tissues of wildlife species.


 Regulations  and  Standards

 OSHA  Standard (air)s  1  ag/m3 TWA.
ACGIH Threshold Limit Values;  1 ag/m*
                               3 ag/mj
mg/mj STEL
REFERENCES
AMERICAN CONFERENCE OP GOVERNMENTAL INDUSTRIAL KTCXEHXSTS  (ACGIH).
     1980.  Documentation of the Threshold Limit values.   4th
     •d.  Cincinnati, Ohio.  48S pages

AMERICAN INDUSTRIAL HYGIENE ASSOCIATION  (AIHA).  1978.  Hygienic
     Guide Series.  Phosphoric Acid.  AIHA, Akron, Ohio
Phosphoric acid
Page 2
October 1985

-------
DOOLI,, J.» KLAASSEN, C.D. « and AKDUS, M.O., tda.  1980.  Casarett
     and Doull's Toxicology:  Th« Basic Selene* of Poisons.
     2nd ed,  Macmillan Publishing Co., New York.  778 pages

LYMAN, W.J., REEHL, W.P., And ROSENBLATT, D.H.  1982.  Handbook
     of Chemical Property Estimation Methods:   Environmental
     Behavior of Organic Compounds.  McGraw-Hill Book Co.,
     New York

THE MERCK INDEX.  1976.  9th ed.  Windholz, M., td.  Merck
     and Co., Rahway, New Jersey

NATIONAL INSTITUTE POR OCCUPATIONAL SAFETY AND HEALTH (NIOSH).
     1984.  Registry of Toxic Effects of Chemical Substances.
     Data Base.  Washington, D.C.  October 1984

SAX, N.I.  1975.  Dangerous Properties of Industrial Materials.
     4th ed.  Van Nostrand Reinhold Co., New York.  1,258 pages

VERSCHUEHEN, X.  1977.  Handbook of Environmental Data on Organic
     Chemicals.  Van Nostrand Reinhold Co., New York.  £59 pages

WEAST, R.E., ed.  1981.  Handbook of Chemistry and Physics.
     62nd ed.  CRC Press, Cleveland, Ohio.  2,332 pages
Phosphoric acid
Page 3
October 1985

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-------
                         PHOSPHORUS (WHITE)
 Summary
      White phosphorous  is highly toxic;  the oral LD,fl  in  the
 rat  is  3 mg/Jcg.  Chronic exposure to phorphorous caases bone
 changes, including bone necrosis.  In humans, this effect occurs
 aore often in the jaws and is termed 'phossy jaw,'  Inhalation
 of phosphorous caused severe respiratory irritation and edema
 in rats.


 CAS Humber:  7723-14-0

 Chemical Formula:  P4

 ICTPAC Naae:  Phosphorus

 Important Synonyms and Trade Names:  Yellow phosphorus, Rat-Nip


 Chemical and Physical Properties

 Molecular Weight:  123.88

 Boiling Point:  280*C

 Melting Pointi  44.1*C

 Specific Gravity:  1.82 at 20*C

 Solubility in Water:  3 ng/liter

 Solubility in Organics:  Soluble in alcohol, ether, chloroform
                          and benezene

 Vapor Pressure:  0.026 ma Ig at 20*C

 Vapor Density:  4.42

 Plash Point:   Spontaneous in air


 Transport and Fate

      Eleaental phosphorus reacts spontaneously with air.  In
 water it is slowly converted to phosphate with the extent of
 conversion dependent on the physical nature of the particular
 •edia.   Phosphorus, as phosphate, is an  essential nutrient
 for plants, and especially for aquatic plants, is often the
 liaiting nutrient.  Therefore, bioaccuaulation of phosphate


 Phosphorus
 Pag« 1
 October 198S

                                                         Ammoemtua
Preceding page blank

-------
by plants is probably an important fatt foe phosphorus In the
environment.


Health Effects

     No information OR the carcinogenicity or autagenicity
of phosphorus was found in the literature reviewed.  Female
rats exposed to as little as 11 Mg/kg of phosphorus on days
1 through 22 of gestation had decreased fertility.

     The most common nonfatal effects of phosphorus are bone
changes, including bone necrosis.  In humans, this effect occurs
aost often in the jaws of occupationally exposed workers and
is termed "phossy jaw.*  phosphorus is highly toxic, with death
reported in a human who ingested a dose of 1 mg/kg.  The oral
LD5Q in the rat is 3 mg/kg.  inhalation by rats of 100 ag/m
called severe respiratory irritation and high aortality due
to bronchopneuaonia or edema.


Toxieity to Wildlife and Domestic Aniaala

     Bluegill sunfish had 48 and 110 hour LC-- values of 105
Mg/liter and 25 pg/liter, respectively.  Adult salaon exposed
to elemental phosphorus concentrations of less than 40 Mg/liter
show signs of extensive heaolysis.  Juvenile Atlantic salaon
exposed to phosphorus bad a 195-hour LC-fl of 0.8
expose  to phosphorus ba  a  195-hour LC-fl of 0.8 Mgliter,
and Atlantic cod had a US-hour LC,Q of'l.i (if/liter.  Pish
bioconcentrate phosphorus to rather high levels  (SO times environ-
mental levels in auscle and  25*000 times water levels in liver}
following fairly short (24 hour) exposure.

     Phosphorus converted to phosphate  is an environmental
problem not because of its toxicity but because of its action
as an essential nutrient.  Low phosphate levels in the aquatic
environment often beneficially liait the growth of algae and
the introduction of excess phosphate causes algal blooms which
reduce the oxygen in the water.  This decrease in oxygen can
cause the death of soae fish and invertebrate species.

     Phosphorus caused toxic effects in pigs exposed to a dose
of 160 mg/kg and bad ainor behavioral effects on ducks at 3 ag/kg.


Regulations and Standards

OSHA Standard (air)i  100 Mi/a3 TWA

AC5IH Threshold Liait Values:  100 |if/«? TWA
                               300 ug/a4 ST2L
phosphorus
Page 2
October 1985

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 REFERENCES

 AMERICAN CONFERENCE OP GOVERNMENTAL INDUSTRIAL HYGIENISTS  (AC<3II).
      1980.  Documentation of tht Threshold Limit Values.   4th
      •d.  Cincinnati, Ohio.  488 pages

 DOULL, J., KLAASSEN, C.D., and AMDUH, M.O., «ds.  1980.  Casarett
      and Doull's Toxicology:  The Basic Science of Poisons.
      2nd ed.  Macmillan Publishing Co., Hew York.  778 pages

 THE MERCK INDEX.  1976.  9th ed.  Windholz, M., ed.  Merck
      and Co., Rahvay, New Jersey

 RATIONAL INSTITDTS POR OCCOTATIONAL SAFETY AND HEALTH (HIOSH).
      1984.  Registry of Toxic Effects of Chemical Substances.
      Data Base.  Washington, D.C.  October 1984

 SAX,  N.I.  197S.  Dangerous Properties of Industrial Materials.
      4th ed.  Van Mostrand Reinhold Co., New York.  1,258 pages

 U.S.  ENVIRONMENTAL PROTECTION AGENCY  (USEPA).  1976.  Proposed
      Quality Criteria for Water.  Office of Water Planning and
      Standards, Criteria and Standards Division, Washington, D.C.

 WEAST, R.E., ed.  1981.  Handbook of Chemistry and Physics.
      62nd ed.  CKC Press, Cleveland, Ohio.  2,332 pages
Phosphorus
Page 3
October 1985

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                             PICRIC ACID
       fierie acid was mutagenic when tested using the Ames assay.
  In humans, exposure his been associated with nausea, abdominal
  pain, pruritus, and skin disorders.
  CAS Number:  88-89-1
  Chemical Formulas  Cg(H02)3H2OH
  IUPAC Kane:  2,4,6-Trinitrophenol
  Important Synonyms and Trade Names:  Carbazotic acid, 2-hydroxy-
                                       1,3,5-trifiitrobenzene,
                                       melinite, nitroxanthic
                                       acid, phenol trinitrate,
                                       piero nitric acid
  Chemical and Physical Properties
  Molecular Weight:  229.11
  Boiling Point:   Explodes at temperatures greater than 300*C
  Melting Point:   122-123*C
  Specific Gravity:  1.763 at 20*C
  Solubility in Hater:  14,000 ag/liter at 20*C
  Solubility in Organies:  Soluble in alcohol, diethyl ether, acetone,
                           benzene, acetic acid, and pyrimidine
  Log Octanol/Hater Partition Coefficientt  Low (approximately 2)
  Vapor Pressurei  1 ma Ig at 195*C
  Vapor Density:   7.91
  Flash Point: 150.0*C
                        s
  Transport and Fata
       There is little available data on the transport and fate
  of  picric acid.  Picric acid has a relatively low vapor pres-
  sure; therefore, volatilisation probably is not an important
  transport process.
  Picric acid
  Page  1
  October 1985
Preceding page blank

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      In  water*  bacteria  degrade picric acid by  reducing  the
 NO,  groups  to NH,.   Kierobial  biodegradation Is probably the
 most important  fate  process  for picric acid In  the environment.
 Picric acid is  transported readily by surface and groundwater
 (Burton  et  al.  1984).  Its adsorption to sediaents and soil
 probably Is not significant.   Picric  acid has an affinity for
 protein,  which  can lead  to its uptake in the tissue of aquatic
 organises.   For example,  the American oyster (Crasaostrea vir-
 ginica)  has shown biphasic uptake with retention In the  tissues
 of approximately 50% (Burton et al. 1984).

      Picric acid can be  netabolized to a small extent in aquatic
 organisms.


 Health Effects
        f,
      No carcinogenic data were available in the literature
 reviewed.   However,  in a study to evaluate its autagenic poten-
 tial, picric acid yielded positive results in both the Ames
 assay and the Base test  using  Droaophila (Gocke et al. 1981).
 NO information  on reproductive toxicity was available in the
 literature  reviewed.

      In humans,  the  ingestion  or percutaneous absorption of
 picric acid aay cause nausea,  vealting, diarrhea, abdominal
 pain, olicuria  anuria, pruritus, and  skin eruptions.  Skin
 disease appears  to be the aost common toxic effect associated
 with  exposure to picric  acid.  For example, an outbreak  of
 henaturia was observed in naval personnel after the dumping
 of some ammunition containing  the acid in their vicinity.  The
 LD-   for picric acid administered orally ranged froa 250 ag/kg
 in cats to  100 ag/kg in  guinea pigs.


 Toxicity to Wildlife and Denestie Animals

     Available  data  for  freshwater species consist of acute
 toxieity tests  on fish,  arthropods, and algae.

     For fish*  the LCT_  was reported  to be 88 ag/liter.   Trout
 were  listed  as  having1'!  perturbation  level of 4 g/liter  after
 SO ainutes.  Of  the  invertebrate species tested, Daphnia  had an
 LCLO of 88 «g/liter  and  a 42-day study on Crassostrea virginiea
 repealed that picric aeid inhibits growth.

     Scenedesaua showed  an LC.a of 240 ag/liter.  Inhibition of
cell multiplication was  noted  It'70 ag/liter in Microeystic
aerugtnoaa.  There were  no data available on saltwater species.

     The Lix . wa* Measured in  pigeons and frogs using subcuta-
neous injections.  It was 200  sjg/ftg for both, suggesting that


Picric acid
Page 2
October 1985

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                        bu we an en* ^^
trial wildlife or domestic animals.  No other studies on the
toxicity of picric acid were found in the literature reviewed.


Regulations and Standards

OSHA Standard  (air):  100 yg/m3 TWA (skin)

ACGIH Threshold Limit Values;  100 ug/m* TWA
                               300 Mf/n  STEL


REFERENCES

BURTON, D.T., COOPER, K.R., GOODFELLOW, W.L., and ROSENBLATT, D.H,
     1984.  Uptake, elimination, and aetabolisa of   C-Picric
     Acid and x C-Picramic Acid in the Aaerican Oyster {Craasos-
     treavirginlea).  Arch. Environ. Contaa. Tozieol. 13:6S3-€64

COCKS, Z., KING, N.T.t ECIRAROT, I.» and WILD, D.  1981.   Muta-
     genicity of cosaetic ingredients licensed by the European
     communities.  Mutat. Sea. 90:91-109

NATIONAL INSTITUTE FOR OCCUPATIONAL SAFETY AND HEALTH (NIOSI).
     1983.  Registry of Toxic Effects of Chemical Substances.
     Data Base.  Washington, B.C.  July 1984

SAX, N.I.  1975.  Dangerous Properties of Industrial Materials.
     4th «d.  van Noatrand Reinhold Co., New York

VERSCHUEREN, X.  1977.  Handbook of Environmental Data on Organic
     Cheaicals.  Van Nostrand Reinhold Co., New York.  659 pages

WEAST, U.S., ed.  1981.  Handbook of Chemistry and Physics.
     62nd ed.  CRC Press, Cleveland, Ohio.  2,332 pages
Picric acid
Page 3
October 1985

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                    POLYCHLORIMATED BIPHENYLS
Summary
     polychlorinated biphenyls  (PCBs) ace very persistent in
the natural environment and are readily bioaccumulated.  In
humans, exposure to PCBs has been associated with ehloracne,
impairment of liver function* a variety of neurobehavioral
symptoms, menstrual disorders, minor birth abnormalities, and
an Increased incidence of cancer.  Experimental aninals exposed
to PCBs expefienced an increased incidence of cancer; reproduc-
tive problems; neurobehavioral degradation; pathological changes
in the liver, stomach, skin, and other organs; and suppression
of inununological function.  PCBs are often contaminated, and
these contaminants may be much more toxic than the PCBs them-
selves.
Background Information

     polychlorinated biphenyls  (PCBs) are complex mixtures
of chemicals composed of two connected benzene rings with 1
to 10 chlorine atoms attached.  The chemical, physical, and
biological properties of these materials depend to a large
degree on the amount and location of the chlorine atoms on
the two benzene ring* of each specific PCS and on the particular
mixture of individual chlorobiphenyls that comprise the mixture.

CAS Humbert  1336-36-3

Chemical Formula;  CgH.Cl^CgH.Cl^

I UP AC Name:  Specific for each polychlorinated biphenyl

Important Synonyms and Trade Name at  PCBs, chlorinated biphenyls
                                     polychlorobiphenyls, Aroclor
                                     Kanecblor, Clophen
Chemical and Physical Properties

Molecular Weightj  189-399*

Boiling Pointt  267"C and" up*

Melting Folnti  S4-310»C*
•Increases with increasing chlorination.


Polychlorinated biphenyls
Page 1
October 1985
                                                  [Ctomcnc AMOCM
  Preceding page Wank

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 Specific Gravity:   1.3  to  1.5  it  20*C*

 Solubility in Watert  0.003-0.$ ag/liter

 Solubility in Organic*i  Soluble  in aost common organic solvents

 Log Octanol/Water  Partition Coefficient!  4-6*

 Vapor  Pressures  10"3-10"5 aa  Ig  at 20«C**

 Henry's  Law Constant*   1Q~3 to -10"5  atB a3/aele


 Transport and Fate

     The transport and  fate of polychlorinated biphenyls has
 been studied  extensively,  and  although  individual chemicals
 vary in  the rates  at which processes  occur, some generalizations
 can be aade about  PCBs  as  a class.  PCBs are  relatively inert,
 and therefore persistent,  compounds,  with low vapor pressures,
 low water solubility, and  high log octanol/water partition
 coefficients.  Despite  their low  vapor  pressures, they have
 a  high activity coefficient in water, which causes a higher
 rate of  volatilisation  than might normally be expected.  Vol-
 atilization and persistence account for the ubiquitous nature
 of  PCBs  in the environment.  Adsorption to the organic material
 in  soil  or sediaents is probably  the  major fate of at least
 the aore heavily chlorinated PCBs.  Once bound, the PCBs aay
 persist  for years  with  slow desorption  providing continuous,
 low-level exposure to the  surrounding locality.  Bioaeeumulation
 of  PCBs  also  occursf with  aost of the compound stored in the
 adipose  tissue of  the body.  PCBs are degraded primarily by
 two routes.   Less  heavily  chlorinated PCBs (aainly the mono-,
 di-, and trichlorinatad PCBs}  can be  blodegraded by soae sail
 aicroorganisas.  PCBs with five or aore chlorines are not meas-
 urably biodegraded.  These heavier PCBs can be photolyxed by
 ultraviolet light.  This process  is extremely slow, but It
 aay be the aost iaportant  degradation process for these very
 persistent compounds.

     Assessing the toxicity of PCBs is  coaplicated by the fact
 that several different aixtures have been produced and distrib-
 uted commercially  and by the presence of highly toxic contam-
 inants in soae coaaerelal  aixtures.   Soae of  these contaainants
 can be foraed  by combustion of PCBs or"  even by high-temperature
 treatment in  service, so that  used materials  may be aore toxic
 than the  coaaercial aixtures whose toxicity has been studied.
 •Increases with increasing chlorination.
"Decreases with Increasing chlorination.
Polychlorinated biphenyls
Page 2
October 1985

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 Health  Effects

      In humans  exposed  to PCBs  (in  the workplace or via  acci-
 dental  contamination of  food),  reported  adverse effects  include
 chloracne  (a  long-lasting, disfiguring skin disease),  impairment
 of  liver function, a variety  of neurobehavioral and affective
 symptoms,  menstrual disorders,  minor birth abnormalities, and
 probably increased incidence  of cancer.  Animals experimentally
 exposed to PCBs have shown most of  the same symptoms,  as veil
 as  impaired reproduction; pathological changes in the  liver,
 stomach, skin,  and other organs; and suppression of immunological
 functions.  PCBs are carcinogenic in cats and mice and,  in
 appropriate circumstances, enhance  the effects of other  carcin-
 ogens.   Reproductive and neurobiological effects of PCBs have
 been  reported in rhesus monkeys at  the lowest dose level tested,
 11  ng/kg body weight/day over a period of several months.


 Toxicity to Wildlife and Domestic Animals

      Polychlorinated blphenyls  are  bioaccumulated and  can be
 biomagnifled.   Therefore, their toxicity increases with  length
 of  exposure and position of the exposed  species on the food
 chain.  The toxicity of  the various PCS mixtures is also depen-
 dent  on their composition.  Because of the complexity  of PCS
 toxicity,  only  general effects  will be discussed here.

      The 96-hour LC50 values  for rainbow trout, bluegills,
 and, channel catfish were around 20  mg/liter.  The same species
 exposed for 10  to 20 days had LC..  values of about 0.1 mg/liter.
 Invertebrate species were also  adversely affected, with  some
 species having  7-day LC-0 values as low  as 1 iig/liter.   in
 general, juvenile organisms appeared more susceptible  to the
 effects of PCBs than either eggs or adults.

      Three primacy ways  in which PCBs can affect terrestrial
 wildlife are outright mortality, adversely affecting reproduc-
 tion, and  changing behavior.  PCS doses  greater than 200 ppm
 in  the  diet or  10 mg/kg body weight (bw) caused some mortality
 in  sensitive bird species exposed for several days.  Doses
 around  1,500 ppa (diet) or about 100 mg/kg (bw) caused extensive
mortality  in these sensitive  species.  They generally caused
 some  mortality  In all species,  with the  level being dependent
 on  the  length of exposure and the particular PCS mixture.
 Some  mammalian  species vare especially susceptible to PCBs.
 For example, mink died when fed as  little as 5 ppm in  the diet
 (equivalent to  less than 1 mg/kg bw/day).  PCBs caused lower
egg production! deformities; decreased hatehability, growth,
 and survival; and some eggshell thinning in reproductive studies
on  chickens fed doses of 20 ppm in  the diet (1 mg/kg bw).
Mink  fed 1 ppm  in the diet (0.2 mg/kg bw) had lower reproductive
 success, and there are indications  that  an increased incidence


Polychlorinated biphenyls
Page  3
October 1985

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 of  premature  births  in  some marine mamreals was linked to PCS
 exposure.   Behavioral effects on wildlife include  increased
 activity, decreased  avoidance response, and decreased nesting,
 all of  which  could significantly influence survival in the
 wild.

     No toxic effects on  domestic animals other than chickens
 were reported in  the sources reviewed, but susceptible species
 would probably be affected in * similar manner to  laboratory
 animals and wildlife.


 Regulationsand Standards

 Ambient water Quality Criteria  (USEPA) i

     Aquatic  Life

     Freshwater

          Acute tozicityi  2 uf/liter
          Chronic toxicityi  0.014 ug/liter

     Saltwater

          Acute toxicityt  10 uf/liter
          Chronic toxicityt  0.030

     HumanHealth

     Estimates of the carcinogenic risks associated with lifetime
     exposure to various  concentrations of PCBs in water are:
                                                              >
         Risk                   Concentration

         10~f                   0.79 nf /liter
         10 5                   0.079 ng/liter
         10"7                   0.007S nf/liter

 CAS  Unit Risk (USEPA)t  4.34 {mg/kg/day}"1

 NIOSH Recommended standards  1.0 u§/»3 TWA

 ACGIH Threshold LUit Valuet  0.5 *g/B3 TWA
AMERICAN CONFERENCE Of COVIRMMENTAL INDUSTRIAL HYCIENISTS  {ACGIH)
     1980.  Docuaentation of the Threshold Liait Values.   4th
     ed.  Cincinnati, Ohio.  481 pages
Polychlorinated biphenyls
Page 4
October 1985

-------
 INTERNATIONAL AGENCY FOR RESEARCH ON CANCER  (IARC).  1971.
      IARC Monographs on the Evaluation of Carcinogenic Risk
      of  Chemicals  to Humans.  Vol. 18s  Polychlorinated Biphenyls
      and Polybrominated Biphenyls.  World Health Organization,
      Lyon, Franc*.  Pp. 43-103

 NATIONAL ACADEMY OF SCIENCES  (HAS).  1977.  Drinking Water
      and Health.   Safe Drinking Water Committee, Washington, D.C.
      939 pages

 ROBERTS, J.R., RODGERS, D.W. , BAILEY, J.R., and RORJCE, K.A.
      1978*  Polyehlorinated Biphenyls:  Biological Criteria
      for an Assessment of their Effects on Environmental Quality.
      National Research Council of Canada, Ottawa, Canada,
      NRCC NO. 1607?

 U.S.  ENVIRONMENTAL PROTECTION AGENCY (USEPA).  1976.  National
      Conference on Polychlorinated Biphenyls  {November 19-21,
      1975, Chicago, Illinois).  Office of Toxic Substances,
      Washington, D.C.  March 1976.  EPA 560/6-75-004

 U.S.  ENVIRONMENTAL PROTECTION AGENCY (USEPA).  1979.  Water-
      Related Environmental Fate of 129 Priority Pollutants.
      Washington, D.C.  December 1979.  EPA 440/4-79-029

 O.S.  ENVIRONMENTAL PROTECTION AGENCY (USEPA).  1980.  Aabient
      Water Quality Criteria for Polyehlorinated Biphenyls CPCBs).
      Office of Water Regulations and Standards, Criteria and
      Standards Division, Washington, D.C.  October 1980.  EPA
      440/5-80-054

 U.S.  ENVIRONMENTAL PROTECTION AGENCY (DSEPA).  1984.  Health
      Effects Assessment for Polyehlorinated Biphenyls.  Environment-
      Criteria and Assessment Offiee, Cincinnati, Ohio.  September
      1984.  ECAOCIN-H004 (Final Draft)

 U.S.  ENVIRONMENTAL PROTECTION AGENCY {USEPA}.  1985.  Health
      Assessment Document for Dichloromethane  (Metbylene Chloride).
      Office of Health and Environmental Assessment.  Washington,
      D.C.  February 1985.  SPA 600/9-82/004F
Polyehlorinated biphenyls
Page 5
October IfiS
                                                 Oement Ammocmvmm
                      V53

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                     POLXCHLORIHATED DlBENZO-p-DIOXINS
     Summary
          Polychlorinated dibenzo-p-dioxins (PCDDs)  art often found
     as contaminants in chlorinated phenolic compounda.  They persist
     in the natural environment and can be  bioaecunulated.   Exposure
     to PCDDs has been associated with numerous  adverse health effects,
     including cancer, genotoxieity, enzyme induction;  chloracne,
     teratogenicity, reproductive toxicity, immunotoxicity,  porpnyria
     cutanca tardo, and neurobehavioral changes.


     Chemical Formulas  C12H4C1E02

     IUPAC Mame:   Polychlorodibenzo-l,4-dioxins

     Important Synonyms and Trade Names:  Dloxins, PCDDs


     Chemical and Physical Properties

     Boiling Point:  500*C (begin* to decompose)

     Melting Point:  Around 300*C

     Solubility in Hater:   Insoluble

     Solubility in Organics:   Soluble in fats, oils,  and other relatively
                              nonpolar solvents

     Log Oetanol/Water Partition Coefficients  Approximately 5

     Vapor Pressures  ID"6 mm Eg at 25*C


     Transport andfate

          Polychlorinated dibenzo-p-dioxins (PCDDs)  have a very
     low vapor pressure and therefore are unlikely to volatize into
     the atmosphere.  However, there are studies that indicate volati-
     tation my occur.  Experiments have shown PCDDs to be highly
     sorbed to sediments,  soils, and bioata so they  may be transported
     through the air in soil dust.  Because PCDDs are tightly bound
     to soils, it is probable that any surface water  contamination
     found in polluted areas" is from soil erosion rather than from
     leaching.  A calculated sediment/water equilibrium partition     _.
     coefficient using six sets of data for PCDDs varied from 1.1 x 10
     to 2.1 x 10  .  This indicates that most PCDDs  in  water will
     be sorbed to particulates.
     Polychlorinated  dibenzo-p-dioxins
     Page  1
     October  19S5
Preceding page blank

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      PCDDs  do  not  readily  undergo  photodegradation  unless  solvents
 are  present which  will  act as hydrogen donors during  reductive
 dechlorination.  Certain microorganisms have been found  that
 will degrade PCDDs.  The half-life of fCDDs in soil has  been
 found to vary  from 130  days to  several years.  Thus,  PCDDs
 are  persistent in  the environment.


 Health Effects

      Studies of  the  health effects of the PCDDs have  generally
 concentrated on  2,3,7,8-tetrachlorodib«nzo-p-dioxin (TCDD)
 Because  it  is  the  most  toxic of  the PCDDs.  Studies on the
 other PCDDs indicate that  they  cause the saae effects, but
 at different quantitative  doses  than TCDD.

      The  structure-activity relationships aaong the PCDDs are
 reasonable  well-defined.   Isoners  with 2 or fewer chlorine
 atoms in  the 2,  3, 7, and  S positions have low biological activity.
 Isoaers  with 3 or  4 of  these positions substituted have  quantitative!
 and  qualitatively  similar  to biological activity TCDD.   The
 1,2,3/7,  and 8 positions are all only slightly less active
 than TCDD.   Additional  substitutions in the 1, 4* S*  and 9 position."
 considerably reduce  biological  activity.

      A variety of  health effects have been associated or attributes
 to exposure to very  low concentrations of PCDDs, especially
 TCDD in both experimental  aniaals  and humans.  These  effects
 include cancer,  genotoxicity, enzyme induction, teratogenicity
 and  reproductive toxicity,  imaunotoxicity, chloracne, porphyrla
 cutanea  tarda, and neurobehavioral toxieity.  TCDD has been
 shown to  induce  cancer  in  mice  and rats following dermal or
 oral administration.  Animal studies suggest that imnunotoxicity
 is probably the  most potent effect of TCDD.  Both ianunotoxicity
 and  the enzyme inducing effects  of PCDDs are probably mediated
 through a cytosolic  receptor that  high affinity for PCDDs.
 Chloracne is the only clear effect that PCDD intoxication has
 produced  in humans.


 Toxieity to Wildlife and Domestic  Aniaals

      Freshwater  aquatic species  exposed to low concentrations
 of TCDD  (in the  parts per  trillion range) foe 4 days  displayed
 toxic signs and  died from  40 to  140 days later.  Acute toxic
 effects were not noted ,in  many of  tbe aquatic species at the
 level of TCDD  water solubility,  0.2 ug/liter.  Borses exposed
 to TCDD in  contaminated waste oil  used to control dust in corrals,
 became sick and  died*
Polychlorinated dibenio-p-dioxins
Page 2
October 1985

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 REFERENCES

 NATIONAL  INSTITUTE FOR OCCUPATIONAL SAFETY AND HEALTH  (NIOSHJ.
      1983.  Registry of Toxic Effects of Chemical Substances.
      Data Base.  Washington, D.C.  October 1983

 U.S.  ENVIRONMENTAL PROTECTION AGENCY  (USEPA).  1979.  Water-
      Related Environmental Pate of 129 Priority Pollutants.
      Washington, D.C.  December 1979.  EPA 440/4-79-029

 U.S.  ENVIRONMENTAL PROTECTION AGENCY  (USEPA).  1984.  Ambient
      Hater Quality Criteria for Tetrachlorodiben»o-p-dioxin.
      Office of Water Regulations and Standards, Criteria and
      Standards Division, Washington, D.C.  February 1984.
      EPA  440/5-840-007

 VETERANS  ADMINISTRATION  (VA).  1981.  Review of Literature on
      Herbicides Including Phenoxy Herbicides and Associated
      Dioxin.  Vols. 1 and 2:  Analysis of Literature.  Depart-
      ment of Medicine and Surgery, Washington, D.C.

 VETERANS  ADMINISTRATION  (VA).  1984.  Review of Literature
      on Herbicides, Including Phenoxy Herbicides and Associated
      Dioxins.  Vols. 3 and 4t  Analysis of Recent Literature on
      Health Effects.  Department of Medicine and Surgery* Wash-
      ington, D.C.
Polychlorinated diben*o-p-dioxins
Page 3
October 198S

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                  POLYCYCLIC AROMATIC HYDROCARBONS
 Summary

      Polycyclic aromatic hydrocarbons (PAHs)  act rather persis-
 tent in the environment.  Some PAHs are carcinogenic, causing
 tumors both at the site of application and aystemically.  The
 carcinogenic PARS are generally active in mutsgenlc assays.
 They also cause skin disorders and Immunosuppression.  Adverse
 effe.cts on the liver and kidney have been associated with expo-
 sure to PAHs 'in general.
 Important Synonyms and Trade Names:   Polynuclear aromatic hydro-
                                      carbons, PAH,  PMA


 Chemical and Physical Properties

      The polycyclic aromatic hydrocarbons are a class oC compounds
 consisting of substituted and unsubstituted polycyclic aromatic
 rings formed by the Incomplete combustion of organic materials.
 Their chemical, physical, and biological properties vary with
 their size and shape.


 Molecular Weights  116-278

 Melting Points  8Q*C-270*C*

 Specific Gravity?  1.1-1.3 at 2Q*C*

 Solubility in Water*   0.0003-34 ag/liter**

 Solubility in Organicsi   Soluble In  most common organic solvents

 log Octanol/Water Partition Coefficient;  3.4-7.6*

 Vapor Pressure:  Ifl"10 to 10*2 mm Eg at 20*C*»
  •Generally Increases with incraasing molecular weight.
 ••Generally decreases with Increasing molecular weight.
 Polycyclic aromatic hydrocarbons
 Page  1                                          ~
 October  1985                                   ||JCl«m*nt AMOOB&M
Preceding page Wa^

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 Transportand  Pate

      Very little  information  on  specific  polycyclic  aromatic
 hydrocarbons  (PAHs)  is  available.  The  environmental fate  and
 transport of  these  compounds  art largely  Inferred  from data on
 benzo(a)pyrene and  mixtures ofPAS*.  The relatively high  log
 octanol/water  partition coefficients of PAHs  indicate that they
 should  be strongly  adsorbed onto suspended particulate matter,
 especially participates high  in  organic content.   The available
 information suggests that  these  compounds can accumulate in the
 sediment  and biota  portions of the aquatic environment and that
 adsorption is'probably  the dominant aquatic transport process.
 Atmospheric transport of PAHs is also possible.  This generally
 occurs  by adsorbtion onto  airborne particulate natter* but some of
 the  PAHs  with  relatively low  molecular  weights are volatile.
 Regardless of  the method of atmospheric transport, PASS are re-
 turned  to aquatic and terrestrial systeas by  atmospheric fallout
 or precipitation.   They can also reach  ground or surface waters by
 leaching  from  polluted  soils.

      PAHs are  relatively Insoluble in water/  but the dissolved
 portion nay undergo rapid, direct photolysis.  Singlet oxygen is
 the  oxidant, and quinones  are the products in these  reactions.
 Oxidation by chlorine and  ozone  may be  an iaportant  fate process
 when these oxidants  are available in sufficient quantities.

      Although  polycyclic aromatic hydrocarbons are rapidly bio-
 aecumulated, they are also quickly metabolized and eliminated from
 most organisms (shellfish  are a  known exception).  Bioaccuaula-
 tion, especially in  vertebrate organisms, is  usually short tern,
 so it is  not considered an important fate process  in multieellular
 organisms.  Biodegration and  biotransformation are probably the
 ultimate  fate  processes for PAHs,  The  available data suggest that
 the  PAHs  with  high molecular  weights are  degraded  slowly by
 microbes  and readily metabolized by multieellular  organisms.
 Microbes  appear to degrade PAfla  much more completely than  mammals.
 Biodegradatlon probably occurs more slowly in aquatic systems than
 in soil,  and it may  be  much more Important in systems that are
 chronically affected  by PAH contamination*


 Health  Effects

     The  potential  for  PAfls'to induce malignant transformation
 dominates the  consideration of health hazards resulting from
 exposure,  because there often are no overt signs of  toxicity until
 the  dose  Is high enough to produce a high tumor incidence.  The
 attached  table contains lARC's classification of some PAHs accord-
 Ing  to  their carcinogenlcity.

     No case reports  or epidemological  studies concerning  the sig-
 nificance of human exposure to individual PAHs are available.
Polycyclic aromatic hydrocarbons
Page 2
October 1985

-------
However, coal tar and other Materials known to be carcinogenic to
humans contain PAHs.

     PAHs administered by various routes have bean found to be
carcinogenic in several animal species and to have both local and
systemic carcinogenic effects.  On oral administration, carcino-
genic PAHs produce tumors of the forestoaach in mice.  Lung tumors
are produced in hamsters after intratracheal administration and in
aice after intravenous administration.  In skin painting experi-
ments with mice, carcinogenic PAHs produced skin carcinomas.
Other observed effects include induction of local sarcomas and an
increased incidence of lung adenomas in mice following single,
subcutaneous injections.  Studies in other specias, while indicat-
ing that PAHs have universal carcinogenic effects, are less com-
plete.  Carcinogenic PAHs are reported to be mutagenic in a vari-
ety of test systems.  The limited available information suggests
that PAHs are not very potent teratogens or reproductive toxins.

     There is very little Information regarding nonmalignant
changes caused by exposure to PAHs.  Application of carcinogenic
PAHs to mouse skin is reported to cause destruction of sebaceous
glands, hyperplasia, hyperkeratosis, and ulceration.  Many carcin-
ogenic PAHs also have ioaunosuppressive effects.  Subcutaneous in-
jections of some PAHs for several weeks reportedly caused hemo-
lymphatic changes in the lymph nodes in rats.  Workers exposed to
FAH-containing materials have exhibited chronic dermatitis,
hyperkeratoses, and other skin disorders.

Toxicity to Wildlife and Domestic Animals

     There is very little information on the environmental toxic-
ity of PAHs;  they probably are not very toxic to aquatic organ-
isms*


Regulations and standards

Ambient Water Quality Criteria (OSEPA)i

     Aquatic Life

     The available data are not adequate foe establishing cri-
     teria.

     Hunan Health
                       •^
     Estimates of the carcinogenic risks associated with lifetime
     exposure to various concentrations of carcinogenic PAHs in
     water are:
Polycyclic aromatic hydrocarbons
Page 3
October 1985                                    Oo.rn.nt: AMOO«C««

-------
      Risk                        Concentration
                                 28.0 ng/littr
                                 2.8 ng/lit«r
                                 0.28
CXG Unit Risk  (USEPA)i  B«nzo(a)pyr*ne:  11.5  (mg/teg/day)"1
Polycyclie «roaatic hydrocarbon*
Pag« 4
October 1985

-------
                     CARCXHOGENICITY OF PAHS
     Ch«nical§ for which there is sufficient evidence that they
•re carcinogenic  in animals:
Benzo(a)anthracene
Benzo{b}fluoranthene
Benzo(j)fluoranthene
Benzo(k)fluoranthene
Benzo(a)pyrene
Dibenzo(a,h)acridine
Dibenzo(a,j)acridine
Dibenzo(a,h Janthracene
                    7H-Dibenzo(c,g}carbazole
                    Dibenzo(a,e)pyrene
                    Dibenzo(a,hjpyrene
                    Dibenzo(a,i)pyrene
                    Dibenzo(afl)pycene
                    Indeno(1,2,3-c»d)pyrene
                    5-Methylchrysene
     Chemicals for which there is limited evidence that they
are carcinogenic  in animals:
Anthranthrene
Benzo(c}acr id ine
Carbazole
Chrysene
Cyclopenta(c,d)pyrene
                    Dibenzo(a,c)anthracene
                    Dibenzo(a,j)anthracene
                    Dibenzo(a ,e)fluoranthene
                    2-»  3-»  4-»  and  fi-Methylchrysene
                    2- and 3-Methylfluoranthene
     Chemicals for which the evidence is inadequate to assess
their carcinogenicity:
Benzo(a)acridine
Benzo(g,h,i)fluoranthene
Benzo (a)fluorene
Benzo (b)fluorene
Benzo {c)fluorene
Benzo (g,hfijperylene
Benzo(c)pnenanthrene
Benzo(e)pyrene
                    Coronene
                    If 4-Dimethylphenanthr ene
                    Fluorene
                    1-Methylchrysene
                    1-Methylphenanthrene
                    Perylene
                    Phenanthrene
                    Triphenylene
     Chemicals for which the available data provide no evidence
that they are carcinogenic:
Anthracene
Fluoranthene
                    Pyrene
SOURCE:  IARC 1983
Polycyclic an
Page S
October 1985
latic  hydrocarbons

-------
 REFERENCES

 INTERNATIONAL AGENCY FOR RESEARCH ON CANCER  (IARC).  1983.
      IARC Monographs on the Evaluation of Carcinogenic Risk
      of  Chemicals  to Huaans.  Vol. 32:  Polynuciear Aromatic
      Compounds;  Part 1, Chemical, Environmental, and Experimental
      Data.  World  Health Organization, Lyon, franc*

 NATIONAL INSTITUTE FOR OCCUPATIONAL SAFETY AMD B2ALTB (HIOSH).
      1984.  Registry of Toxic Effects of Chemical Substances.
      Data Base.  Washington, D.C.

 SANTODONATO, J., HOWARD, P., and BASE, 0.  1981.  Health and
      ecological  assessment of polynuclear aromatic hydrocarbons.
      J.  Environ. Pathol. Toxicol. 5:l-3§4

 U.S.  ENVIRONMENTAL PROTECTION AGENCY  (DSEPA).  1979.  Water-
      Related Environmental Fate of 129 Priority Pollutants.
      Washington, D.C.  December 1979.  EPA 440/4-79-029

 U.S.  ENVIRONMENTAL PROTECTION AGENCY  (USEPA).  1910.  Ambient
      Water Quality Criteria for Polynuclear Aroaatic Hydrocarbons
      Office of Water Regulations and Standards, Criteria and
      Standards Division, Washington, D.C.  October 1980.  EPA
      440/5-80-069

 U.S.  ENVIRONMENTAL PROTECTION AGENCY  (USEPA).  1984.  Health
      Effects Assesaaeat for Polycyclic Aromatic Hydrocarbons.
      Environmental Criteria and Assessment Office, Cincinnati,
      Ohio.  September 1984.  ECAO-CIN-H013 (final Draft)

 U.S.  ENVIRONMENTAL PROTECTION AGENCY  (USEPA}.  1985.  Health
      Assessment Document for Dichloroaethane (Nethylene Chloride)
      Office of Health and Environmental Assessment, Washington,
      D.C.  February 1985.  EPA 600/8-82/004F

 WEAST, R.S., ed.   1981.  Handbook of Chemistry and Physics.
      62nd ed.  CRC Press, Cleveland, Ohio.  2,332 pages
Polycyclic aromatic hydrocarbons
Page €
October 1985

-------
                             SELENIUM
Summary

     Although selenium is an essential element, exposure to
amounts just slightly above the required levels can produce
toxic effects.  Signs of chronic exposure in humans include
dermatitis, neurobehavioral effects, gastrointestinal disturb-
ances, dental caries and discoloration, and partial loss of
hair and nails.  Toxic effects observed in animals include
degeneration'of the liver, kidneys, and myocardia; hemorrhages
in the digestive tract; and brain damage,  inhalation of selenium
irritates  the eyes, nose, and throat.
Background Information

     Selenium is stable in four valence states: -2, 0, +4, and
4-6.  Elemental selenium can bt considered inert in the aquatic
environmentf and deposition of this fora appears to be a major
sink for selenium in natural systems.

CAS Numberi  7732-49-2

Chemical Formula:  S*

IUPAC Namei  selenium


Chemical and Phyaica1;Properties *

Atomic Weightt  73.96

Boiling Points  684.9*C

Melting Point:  217*C

Specific Gravityj  4.26 to 4. SI

Solubility in Water:  Insoluble

Solubility in Organicst  Crystals slightly soluble in carbon
                         disulfide, soluble in ether; amorphous
                         forms soluble in carbon disulfide,
                        ^methylene iodide, benzene, and quincline
Selenium
Page 1
October 198S                                   __,
                                                 LO«m
-------
 Transport  and  Fate

      In  aerobic waters  and  at high pH» selenium  is present
 In  the aelenite  (4-4} or selenate  (+6) oxidation  state.  These
 chemical .species  are very soluble, and it is probable that
 moat  of  the selenium released Into the aquatic environment
 la  transported in these forms to  the oceans.  Under reducing
 conditions and at low pi, elemental selenium or  netal selenides
 can be formed,  similar chemical  speciation patterns affect
 the.transport  of  selenium in soil,  in poorly aerated, acidic
 soils., insoluble  forms  predominate.  In well-aerated, alkaline
 soils, soluble forms of selenium  subject to leaching and com-
 pounds readily taken up by  plants tend to be formed.

      Selenium  is  strongly adsorbed to hydrous metal oxides,
 while clays and organic materials have a lesser  affinity.
 Sorption by bed sediments or suspended solids, and precipitation
 with  hydrous iron oxides are probably the major  control on
 mobility of selenium in aerobic waters.  However, most selenium
 in  aquatic systems Is probably transported as the dissolved
 species.   Experimental  studies indicate that selenium is quite
 mobile in  clays*  especially under alkaline conditions.

      Selenium  is  bioaeeumulated by aquatic and terrestrial
 organisms.  Although dietary intake- is thought to be the most
 important  source  of selenium In many organisms,  little biomagnifl-
 cation appears to take  place.  Conversion of selenium to inert
 and insoluble  forms may occur in  terrestrial and aquatic orga-
 nisms.  However,  selenium can be  methylated by a variety of
 organisms, including benthic microflora.  In a reducing envi-
 ronment, hydrogen selenide  (H-Se) may be formed.  Both the
 methylated forms  and H.Se are volatile, and can  be released
 to  the atmosphere.  Consequently* remobilixation of selenium
 from  aquatic and  terrestrial systems, through biotransformation
 to volatile forms and subsequent  atmospheric transport, can
 result in  significant recycling.


 Health iffeets

      There is  no  evidence that selenium is carcinogenic in
 huaans.  Selenium has been  tested by the oral route in experi-
mental animals, but the available data are insufficient to
 allow unequivocal evaluation of its carcinogenic potential.
However, recent reports suggest that selenium is not carcino-
 genic.  Several studies have shown that selenium may actually
 reduce the incidence of tumors under certain conditions.  Muta-
genlclty, teratogenlclty, and reproductive effects have not
been  adequately tested.

      Selenium  is  an essential element In animals and probably
 in humans.  However, exposure to  amounts only slightly above


Selenium
?age  2
October 1919

-------
the required! levels can produce acute and chronic toxic effects.
Acute toxicities of *eleniun compounds vary greatly, while
the chronic effects of most forms are similar.  Exposure nay
be by oralf inhalation, or dermal routes, and effects in humans
and experimental animals are similar.  Acute effects include
degeneration of liver, kidneys, and myocardia, hemorrhages
in the digestive tract, and brain damage.  Eye, nose, and throat
irritation may also occur with inhalation exposure.  The acute
oral LDeQ value of sodium selenite in rats vas approximately
10 mg/kg.  Chronic toxicity in humans appears to occur only
in areas where foods containing excessive concentrations of
selenium are ingested.  Signs of chronic intoxication include
depression, nervousness, dermatitis, gastrointestinal distur-
bances, dental caries and discoloration, lassitude, and partial
loss of hair and nails.


Toxicity to Wildlife and Domestic Animals

     Some food and forage crops growing on certain seleniferous
soils can accumulate selenium to concentrations as high as
1,000 ppa.  Chronic selenium toxicity can occur in grazing
animals that consume plants containing 3 to 25 ppm over a long
period of time.  Symptoms of chronic poisoning ("alkali" disease)
include lack of vitality, loss of hair, sterility, hoof defor-
mity, lameness, anemia, and fatty necrosis of the liver.  Acute
toxic effects including impairment of vision, weakness of limbs,
and respiratory failure may occur in livestock consuming 100
to 1,000 ppm of selenium.  There are reports that consumption
of plants containing 400 to 800 ppm has been lethal to sheep,
hogs, and calves*  There are no reports of increased cancer
rates among livestock in seleniferous areas.


Regulations andStandards

Ambient water Quality criteria (USZPA)t

     Aquatic Life (Selenite}

     Freshwater

       Acute toxicityi  260 ug/liter
       Chronic toxicity:  35 ug/liter

     Saltwater
                      \
       Acute toxicity:  410 ug/liter
       Chronic toxicityi  54 ug/lit«r

     Ho criteria for the protection of aquatic life were established
     for selenate.


Selenium
Page 3
October 1915

-------
      Huaan  Health

      Criterion;  10  tig/liter

 Primacy Drinking Water  Standard:   0.01 ag/liter

 NIOSH Recommended  Standard:  0.2 «g/a  TWA  (S« compounds, as Se)

 OSHA  Standard:  0.2  mg/n  TWA  (Se  compounds, as Se)


 REFERENCES

 AMERICAN CONFERENCE  OF  GOVERNMENTAL  INDUSTRIAL IYGIENISTS (ACGIH),
      1980.  Documentation of the Threshold Limit Values.  4th
      ed.  Cincinnati, Ohio.  488 pages

 DOCLL,  J.,  RLAASSEN, C.O., and AMDCR* M.O., eds.  1980.  Casarett
      and Doull'i Toxicology:  The  Basic Science of Poisons.
      2nd ed.  Macmillan Publishing Co., Heir fork.  778 pages

 INTERNATIONAL AGENCY POX RESEARCH  OH CANCER  (IARC).  1975.
      IARC Monographs on the Evaluation of Carcinogenic Risk
      of Chemicals  to Man.  Vol. 9s   Some Aziridines, N-, S-,
      and  0-Mustards, and Selenium.   World Health Organization,
      Lyonr  Prance.  Pp. 245-250

 NATIONAL  INSTITUTE fOR  OCCUPATIONAL  SAFETY AND HEALTH  (NIOSH).
      1984.  Registry of foiic Effects of Chemical Substances.
      Data Base.  Washington, D.C.  January 1984

 SAX,  N.I.   1975.  Dangerous Properties of Industrial Materials.
      4th  ed.  Van Nostrand Reinhold  Co., New York.  1,258 pages

 U.S.  ENVIRONMENTAL PROTECTION AGENCY (USEPA).  1979.  Water-
      Related Environmental Pate of 129 Priority Pollutants.
      Washington, D.C.   December 1979.  EPA 440/4-79-029

 U.S.  ENVIRONMENTAL PROTECTION AGENCY (USEPA).  1980.  Ambient
      Water  Quality Criteria for selenium.  Office of Water
      Regulations and Standards, Criteria and Standards Division,
      Washington, D.C.   October 1980.  SPA 440/5-80-070

 U.S.  ENVIRONMENTAL PROTECTION AGENCY (USEPA).  1984.  Health
      Effects Assessment^ for Selenium.  Environmental Criteria
      and Assessment Office, Cincinnati, Ohio.   September 19S4.
      ECAO-CIN-H058   (final Draft)

WEA5T, R.E., ed.  1981.  Handbook  of Chemistry and Physics.
      62nd ed.  CRC Press, Cleveland, Ohio.  2,332 pages
Selenium
Page 4
October 1985

-------
                              SILVER
Summary
     Exposure  to high levels of silver can cause argyria (an
 impregnation of the  tissues) and lesions of the liver, kidney,
 bone marrow, and lungs in humans.  Liver and kidney damage,
 central nervous system effects, and pulmonary edema and congestion
 have~"been reported in experimental animals exposed to various
 silver compounds.
CAS Numbers  7440-22-4

Chemical Formulas Ag

IUPAC Namei  Silver


Chemical and Physical Properties

Atomic Weight!  107.868

Boiling Point!  2212*C

Melting Point:  961.93*C

Specific Gravity:  10.5 at 20*C

Solubility In Watert  Insoluble  (some compounds are soluble)

solubility In Organicsi  Soluble la alkali cyanide solutions


Transport .and Pate

     Silver can exist In several chemical forms In aqueous
systems.  Metallic silver, which has very low solubility, Is
stable over much of the Eh-pH range for water.  Concentrations
of hydrated silver cations, usually present as the univalent
species, may be controlled by reaction with chloride, bromide,
and iodide Ions to five insoluble silver halldes.  Precipitation
of AgCl may exert a major control on solubility of silver where
chloride concentrations are relatively high.  Under the reducing
conditions often found In bed sediments, formation of insoluble
silver sulfides and metallic silver may also control levels
of soluble silver species.  Silver is strongly sorbed by mangan-
ese dioxide, ferric hydroxide, and clay minerals.  Sorption
is probably the dominant process leading to removal of dissolved



Silver

October 19SS                                   Qdwmrx Am*QC,mt~

-------
 silver  Iron  the  water  column.   In general, concentrations of
 silver  act higher  in the bed sediments than in overlying waters.
 For  example,  thtst concentrations were reported to differ by
 a  factor of  1,000  in an alpine  lake.

      iioaecumulation of silver  by aquatic plants, invertebrates,
 and  vertebrates  occurs readily  and appears to depend primarily
 on sorption/desorption fron sediments.  However, the amount
 of silver partitioned  to the biota appears to be minor in com-
 parison with  the amount partitioned to the sediments.  Little
 fooa*-chain magnification seeas  to occur.  Photolysis, volatili-
 zation, atmospheric transport,  and biotransformation do not
 appear  to be  important fate or  transport processes for silver.


 Health  effects

      Only equivocal evidence exists to suggest that silver
 has  carcinogenic activity in experimental animals.  Silver
 implants and  injected  colloidal suspensions are reported to
 produce tumors or  hyperplasia at the site of application in
 several studies.   However, it is suggested that the effects
 are  due to the physical form of the metal or to its action
 as an exogenous  irritant*  There are no studies to suggest
 that silver is carcinogenic in  hunans.  Silver does not appear
 to have significant autagenic or teratogenic activity in humans
 or experimental  animals.

      Silver can  be absorbed in  humans* by inhalation or ingestion.
 The  most common  and most noticeable effects of excessive absorp-
 tion are a local of generalized impregnation of the tissues
 referred to as argyria.  in cases of argyri*, accumulation
 of silver can result in a blue-gray pigmentation of the skin,
 hair, internal organs, and conjunctiva of the eye*  Large oral
 doses of silver  compounds may produce serious effects in humans.
 For  example, silver nitrate can cause violent abdominal pain,
 vomiting, and convulsionst and  ingestion of 10 grams is reported
 to usually be fatal.   Lesions of the liver, kidney, bone marrow,
 and  lungs have also been attributed to industrial or medicinal
 exposure.

      Intravenous administration of silver nitrate is reported
 to produce pulmonary edema and  congestion in experimental animals
 Liver and kidney damage, central nervous system effects, and
 death have also  been reported in experimental animals exposed
 to various silver  compounds.  The intraperitoneal LD5Q (30 days)
 for Ag  as the nitrate in male  Swiss albino mice is 13.9 mg/kg.
 Rats exposed to silver in their drinking water for 11 months
shoved no toxic  effects at concentrations less than 0.4 mg/liter.
Hemorrhaging occurred  in the kidneys at 0.4 mg/liter.  Condi-
 tioned reflex activity and immunological resistance were lowered,
 and brain nucleic  aeid content  was increased at 0.5 mg/liter.
Silver
Page 2
October 1985

-------
numerous physiological changes, including growth depression,
and pathomorphological changes in the liver, kidney, stomach,
and small intestine were evident in rats exposed to 20 rag/liter
for 5 aonths.


Toxietty to Wildlife and Domestic Animals

     Acute toxieity values for freshwater invertebrates range
from 0.25 Mf/liter for Paphnia aagna to 4,500 ug/liter for the
scud Gamrnaruspseudolianaeus.  Acute values for fish range from
3.9 ug/liter f6r the fathead minnow in soft water to 280 pg/liter
for rainbow trout in hard water.  In fresh water, the acute
toxieity of silver appears to decrease as hardness increases.
Soluble compounds, such aa silver nitrate, are generally much
aore toxic than insoluble compounds.  Chronic values ranging
frofi 2.S to 29 ug/liter are reported for Daphnia magna.  TWO
early life stage studies with rainbow trout report chronic
values of 0.12 ug/liter.  Acute-chronic ratios for Daphnia
aagna and rainbow trout are 2.0 and 54, respectively.  Fresh
water aquatic plants appear to be aore resistant to silver
than the sore sensitive aniaals.

     Acute values for saltwater organisms range from 4.7 ug/liter
for the summer flounder to 1,400 ug/liter for the sheepshead
minnow.  A chronic value of 18 M9/liter, and an acute-chronic
ratio of 14 is reported for the aysid shrimp.

     Reduced cell numbers are observed in the saltwater alga
Skeletonema costaturn after exposure to 130 ug/liter of silver.

     Excess silver can induce selenium, vitamin !, and copper
deficiency symptoms in animals fed adequate diets, and can
aggravate deficiency symptoms in animals whose diet* lack one
or more of these nutrients.  These effects are reported in
dogs, sheep, pigs, chicks, turkey poults, and ducklings.


Regulations and Standards

Ambient Water Quality Criteria  (USEPA)t

     Aquatic Life

     Freshwater

          Acute toxieity:  e11'72 Hn(hardness)] - 6.52) w/llttr
          Chronic toxieity:  No criteria have been established
     Saltwater

          Acute toxieity:  2.3 ug/liter
          Chronic toxieityt  No criteria have been established
Silver
**9* '
October IfiS


-------
      Hunan Health

      Criterion*  50 |if/llt*c

Primary Drinking Water Standard;  50 Mi/liter

OSHA  Standard:  10 ug/«3 TWA

ACGIH Threshold Liait Valuest  0.1 ag/ffl3.(a«t»l)
                               0.01 »g/»3  {soluble compounds)


REFERENCES

AMERICAN COMPERENCI OP GOVERNMENTAL INDUSTRIAL HYGIZNISTS  (ACGIH).
      1980.  Documentation of the Threshold Liait Values.   4th cd.
      Cincinnati, Ohio.  488 pages

DOOLL, J., RLAASSSN, C.D., and AMDDR, N.O.  1980.  Casarett
      and Doull's Totieologyt  The Basic Science of Poisons.
      2nd ed.  Maenillan Publishing Co., New York.  773 pages

NATIONAL INSTITUTE FOR OCCUPATIONAL SAFETY AND HEALTH (NIOSH).
      1983.  Registry of Toxic Effects of Chemical Substances.
      Data Base.  Washington, B.C.  October 1983

SAX,  N.I.  1975.  Dangerous Properties of Industrial Materials.
      4th ed.  van Nostrand Reinhold Co., Rev York.  1,258  pages

U.S.  ENVIRONMENTAL PROTECTION AGENCY (OSEPA).  1979.  Water-
      Related Environaental Fate of 129 Priority Pollutants.
      Washington, D.C.  D«ceaber 1979.  EPA 440/4-79-029

U.S.  ENVIRONMENTAL PROTECTION AGENCY (0SEPA).  1980.  Ambient
      Water Quality Criteria for Silver.  Office of Water Regula-
      tions and standards, Criteria and Standards Division,
      Washington, D.C.  October I960.  EPA 440/5-80-071

WSAST, R.E., ed.  1981.  Handbook of Cheaistry and Physics.
      82nd ed.  CRC Press, Cleveland, Ohio.  2,332 pages
Silver
Page 4
October 198S

-------
                              SODIOM
Summary

     High doses of certain sodium compounds are reported to
have teratogenlc and reproductive effects in animals.  Several
studies suggest that brain damage and sudden unexpected death
in human infants nay be induced by high sodium levels.  Exposure
to high levels of sodium has also been associated with age-related
increases in high blood pressure in genetically susceptible
individuals.


Background Information

     Sodium is the sixth most abundant element on earth,  it
is very reactive and is never found free in nature.  It reacts
violently with water, decomposing it with the evolution of
R, and the formation of NaOH.  Sodium normally does not ignite
in air at temperatures below 11S*C, but it may ignite spontaneous!
on water.  Because of its reactivity, sodium must be handled
with great care, and contact between it and water and other
substances with which it reacts should be avoided.

CAS Number:  7440-23-5

Chemical Formulai  Ha

IUPAC Name:  Sodium


Chemical and Physical Properties

Atomic Weights  22.9898

Boiling Point:  882.9*C

Melting Point:  97.81*C

Specific Gravityt  0.97

Solubility in Haters  Metal decomposes explosively in water;
                      many sodium compounds are soluble
Transport and Fate

     Many sodium compounds ire soluble in water* and the sodium
ion is readily transported in surface water, soil, and ground-
water.  The extent of sodium transport in soil is dependent,
Sodium

October 1985

-------
 to soae  extent, en  the  cation exchange capacity of the soil.
 Atmospheric  transport of sodium occurs readily.  Evaporation
 of ocean spray particles and! their subsequent incorporation
 into  precipitation  is an important sodium cycling process.
 Sodium is ubiquitous  in nature and is in important component
 of all ecosystems.


 Health Effects

      There is no  evidence  to suggest that sodiua has carcinogenic
 or autagenic effects in humans or experimental animals.  Sodium
 chloride is  reported to produce teratogenic and reproductive
 effects  in experimental animals exposed to high doses by various
 routes.   For example, mice exposed subcutaneously to over 2,000 mg/kc
 of sodium chloride  on day  10 or 11 of gestation had an increased
 incidence of dead or resorbed young*  Live young in this study
 had decreased body  weights and an increased incidence of appendi-
 eular malformations, such  as clubfoot and deviation of the
 digits (Hiahiauri and Miyamoto 1969}.

      Zn  humans, adverse effects of sodiua occur as a result
 of ingestion of excess  amounts of this eleaent*  Acute effects
 appear to occur only in neonates and young infants.  Several
 studies  suggest that permanent brain damage and sudden/ unexpected
 deaths of infants between  the ages of 2 weeks and 2 years nay
 be due to hypernatreaia.   Sodiua produces toxic effects and
 can cause death in  experimental animals exposed to high concen-
 trations.  For example, the oral LD-n value for Had in rats
 is 3,000 ag/kg.                    50

      Clinical and epideaiological studies suggest that ingestion
 of excess sodiua  may contribute to the development of age-related
 increases in blood  pressure and hypertension in genetically
 susceptible  persons.  Studies with experimental aniaals support
 the contention that excess sodiua ingestion is related to the
 development  of hypertension.  If is estiaated that at least
 40 percent of the population would benefit if consumption of
 sidua were limited  to 2,000 ag/day or less.  The sodiua present
 in drinking  water contributes to the total daily intake of
 this  eleaent.  One  survey, which saapled the water supplies
 used  by  about half  of the  U.S. population, reported sodiua
 ion concentrations  ranging froa 0.4 to 1,900 ag/liter.
                        \

Yoxicity to wildlife and Domestic Aniaala

      Although few studies  documenting effects are available,
high  concentrations of  sodiua chloride probably have detrimental
effects on aquatic  organisms and terrestrial plants.  In lakes,
increased salinity will cause stratification and thereby delay
the spring turnover that oxygenates the lower levels of the
Sodiua
Page 2
October 1»SS                      .
                                 '-

-------
lake.  In addition, salinity changes due to high sodium chloride
concentration! nay adversely affect aquatic systems by changing
the osmotic pressure and by increasing the nobility of some
heavy aetals such as aercury.  In terrestrial systems, high
sodium chloride concentrations caused by road deicing have
proved fatal to roadside vegetation, and the increased soil
salinity associated with irrigation has rendered cropland unus-
able.


Regulations and Standards

Department of Transportation;  Flammable solid; dangerous when
                               vet


REFERENCES

NATIONAL ACADEMY OF SCIENCES (HAS).  1977.  Drinking Hater
     and Health.  Safe Drinking Water Committee, Washington,
     D.C.  939 pages

NATIONAL INSTITUTE FOR OCCUPATIONAL SAFETY AND HEALTH (NIOSH),
     19S4.  Registry of Toxic Effects of Chemical Substances.
     Data Base.  Washington, D.C.  July 1984

NISBET, i.c.T.  1974.  Salt on the earth.  Technol. Rev.
     May 1974, pp. €-7

NISHIMOTO, H., and MIYAMOTO, 3.  1969.  Teratogenic effects
     of sodium chloride in mice.  Acta Anat. 74:121-124

RAND, G.M., and BARTHALMOS, G.T.  1980.  Case history:  Pollution
     of the Rhine River.  In Guthrie, F.E., and Perry, J.J.,
     eds.  Introduction to Environmental Toxicology.  Elsevier/North
     Holland, New York.  Pp. 238-240

SAX, N.I.  197S.  Dangerous Properties of Industrial Materials,
     4th ed.  Van Nostrand Reinhold Co., New York.  1,258 pages

WEAST, R.S., ed.  1961.  Handbook of Chemistry and Physics.
     €2nd ed.  CRC Press, Cleveland, Ohio.  2,332 pages
Sodium
Page 3
October 1985

-------

-------
 Summary

      Sodium chlorate yielded positive results in two mutagenicity
 assays.  It Is a strong oxidizing agent and  consequently is
 a fairly potent Irritant.


 CAS Number:  7775-09-9

 Chemical Formula:   NaClO.

 IUPAC Name:  Sodium chlorate

 Important Synonyms and Trade Names:   Asex, Atlacide, chlorate  of
                                      soda, chlorate  salt,  Klorex
                                      Kuaatol, soda chlorate


 Chemical and  physical Properties

 Molecular Weight:   101.44

 Boiling Points   Decomposes  at 300*C

 Melting Points   248*C to 2€1*C

 Specific Gravity:   2.5 mt 20*C

 Solubility in Waters   Approximately  1,000 mg/Uter

 Solubility in Otganics:  Soluble  in  alcohol  and  glycerol


 fransport and fate

      No inforaation on the  transport and fate of sodium  chlorate
 was  found in  the sources reviewed.   Sodium chlorate  is a strong
 oxidizing agent and probably re»ets  quite rapidly in the environ-
 ment.   It is  not likely to  be persistent in  nature.


 flealth  iffeets

      No inforaation on the  earcinogenicity of sodium chlorate
 was  found in  the sources reviewed.   Goefce et al.  (1981)  reported
 that the results of two mutagenicity assays—the Ames assay
 and  the BASC  test  on Prosophila—-were positive for sodium  chlor-
 ate.  No inforaation on the chronic  toxicity of  sodium chlorate
 was  available in the  sources reviewed.   Sodium chlorate  is
 a strong oxidizing agent and therefore is a  fairly strong

 Sodium  chlorate
 Page 1
 October 198S
                                                  [Oemenc Asaeciecee
Preceding page blank

-------
 irritant.  The oral £>D.Q  in rata  ia  1,200 mg/kg, but doses of
 around  200 mg/kg were  fatal to human children,


 Toxic!tv  to Mildlife and  Domestic Animals

      Sodium chlorate was  reported to be toxic to fish, but
 no dose levels were provided.  This  compound is a nonselective
 herbicide.  Mo other information  on  the toxieity of sodium
 chlorate  to wildlife and  domestic animals was found in the
 sources reviewed.


 Regulations and Standards

      No regulations or standards  for sodium chlorate have been
 established.
REFERENCES

DOULL, J., KLAASSEN, C.D., and AMDUR, M.O., eds.  1980.  Casarett
     and Doull's Toxicology:  The Basic Science of Poisons.
     2nd ed.  Macaillan Publishing Co., Sew York.  778 pages

COCKS, S., XING., M.T., 1CXIARDT, I., and WILD, D.  1181.
     Mutagenicity of cosmetic ingredients licensed by the Euro-
     pean Communities.  Mutat. Res. §0if1-109

HERBICIDE HANDBOOK Of THE WEED SCIENCE SOCIETY OF AMERICA.
     1979.  4th ed.  WSSA Herbicide Handbook Committee, Champaign,
     Illinois.  Pp. 416-418

TIE MERCK INDEX.  1976.   9th ed.  Windholz, M., ed.  Merck
     and Co.* Rahway, New Jersey

NATIONAL INSTITUTE FOR OCCUPATIONAL SAFETY AND HEALTH (NIOSH).
     1984.  Registry of Toxic Effects of Chemical Substances.
     Data Base.  Washington, D.C.  October 1984

SAX, N.I.  197S.  Dangerous Properties of Industrial Materials.
     4th ed.  Van Hostrand Reinhold Co., Sew fork.  1,258 pages

TOXIC AND HAZARDOUS INDUSTRIAL CHEMICALS SAFETY MANUAL.  1976.
     The International Technical Information Institute, Tokyo,
     Japan               v

USAST, R.S., ed.  1981.  Handbook of Chemistry and Physics.
     (2nd ed.  CRC Press, Cleveland, Ohio.  2,332 pages
Sodium chlorate
Page 2
October 198S

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                         STQDDARD SOLVENT
     Stoddard solvent is an eye, nose/ and throat Irritant
in humans.  Acute exposure to high vapor concentrations can
cause headaches and produce narcotic effects.  Chronic exposure
to high airborne concentrations of Stoddard solvent Bay produce
kidney damage.


Background Information

     Stoddard solvent is a mixture of 9 to 11 carbon straight
and branched paraffins, cycloparaffins, and aromatic hydrocarbons.
Properties of a specific sample will depend on the composition
of the particular mixture.

CAS Number:  8052-41-3

Chemical Formula:  Predominant molecular species, C9-C11;
                   30-50% straight and branched chain paraffins,
                   30-401 cycloparaffins, and 10-20% aromatic
                   hydrocarbons


Chemical and Physical Properties

Molecular Weightt  135-145 (average)

Boiling Point:  160-210'C

Specific Gravity:  0.75-0.80

Solubility In Waters  Insoluble

Solubility In Organicsi  Miscible with most organic solvents

Vapor Pressures  4.0-4.5 mm Eg at 25*C

Vapor Density:  S

Flash Point*  37.S-«0«C

                      \
Transport and Fate

     Practically no Information concerning the environmental
transport and fate of Stoddard solvent is available.  This
solvent contains a mixture of organic compounds, and each of
these components may behave somewhat differently in the environ-
ment .


Stoddard solvent
Page 1                                        ^
October 19tS                                  Qci*m*ncAMooa««s

-------
      In  general,  the  low water solubility and moderate vapor
 pressure of  Stoddard  solvent suggest that volatilization may
 be  a  significant  transport process.  Although direct oxidation
 in  water is  unlikely, photooxidation of compounds reaching
 the atmosphere may occur.  The solubility of Stoddard solvent
 in  organlcs  and its low water solubility suggest that sorption
 to  suspended particles and bed sediments containing organic
 components may be a significant transport process in aquatic
 systems* Sorption to organic materials may limit the movement
 of  Stoddard  solvent in soil*  Data concerning other related
 hydrocarbons suggest  that biodegradation by a variety of micro-
 organisms may be  an important environmental fate for Stoddard
 solvent* but that bioaecunulation would not be an important
 long-term process.

      Photolysis and hydrolysis are not likely to be significant
 environmental fates.
Health Effects

     There are no reports of carcinogenicity, mutagenicity,
teratogenicity, or reproductive effects associated with exposure
to Stoddard solvent,  aowever, benzene, a potential human leukerao
genic agent, may be a contaminant of some samples of refined
petroleum solvents.  Stoddard solvent generally contains 0.1%
benzene or less, and it is thought that ordinary use of solvents
containing less than 51 benzene would net produce a benzene
exposure hazard.

     Stoddard solvent is an eyer nose, and throat irritant
in humans and has a dtfatting and irritating action on the
skin.  At relatively high vapor concentrations it can cause
headaches and produce narcotic effects.  Aspiration of the
liquid can produce diffused chemical irritation of the lungs,
resulting in edema; and a few millillters may be fatal in these
incidents.  Inhalation exposure of laboratory aniaals can result
in irritation and narcotic effects.  Chronic exposure to rela-
tively high concentrations (greater than 1,000 mg/m3) may produce
kidney damage, although these results are equivocal.


Toxicltv to Wildlife and Domestie Aniaala
              information to characterize the toxieity of Stoddard
solvent to wildlife and "domestic animals is not available.


Regulations and Standards

moss Recommended Standards  350 mg/m3 TWA
                             1,100 mg/mVlS "in Calling Level
Stoddard solvent
Page 2
October 1985

-------
05WI Standard:  2,950 ag/m3 TWA

ACGIH Threshold Limit Values:  525 ag/n3 TWA
                               1,050 ng/B3 STEL
REFERENCES

AMERICAS CONFERENCE OF GOVERNMENTAL INDQSTRIAL RYGIBNISTS  (ACGXHJ
     19BO.  Documentation of the Threshold Limit Values.   4th
     3d,  Cincinnati, Ohio.  488 pages

NATIONAL INSTITUTE FOR OCCUPATIONAL SAFETY AND HEALTH  (HIOSH5 .
     1977.  Criteria for a Recommended Standard—Occupational
     Exposure to Refined Petroleum Solvents.  DREW Publication
     No. (NIOSH) 77-192

NATIONAL INSTITUTE FOR OCCUPATIONAL SAFETY AND HEALTH  (NIOSH).
     1984.  Registry of Toxic Effects of Chemical Substances.
     Data Base.  Washington, B.C.  January 1984

SAX, N.I.  1975.  Dangerous Properties of Industrial Materials.
     4th ed.  Van Nostrand Reinhold Co., Rev York.  1,258 pages

U.S. ENVIRONMENTAL PROTECTION AGENCY  (DSEPA).  1979.  Wattr-
     Related Environmental Fate of 129 Priority Pollutants.
     Washington, D.C.  December 1979,  SPA 440/4-79-029
Stoddard solvent
Page 3
October 198 S        -                          Oci«m*r« AaKoc.au>

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-------
                          ,S-TTTRACHLOROBENZENE
 Summary
      1,2,4,S-Tetrachlorobenzene caused  slight  liver  toxicity
 and disrupted conditioned reflexes in studies  on  experimental
 animals.   Tetrachlorobenzenes in general  appear  to induce  the
 activity  of  raicrosomal enzymes.
 CAS Number:   95-94-3
 Chemical  Formula:   ^gH^Cl*
 IUPAC Name:   1,2,4,5-Tetrachlorobenzene
 important Synonyms and Trade Names:   Benzene tetrachloride
 Chemical  and Physical Properties
 Molecular weights   215.9
 Boiling Pointi   245*C
 Melting Points   139.S*C
 Specific  Gravity:   1.734
 Solubility in Water:  Insoluble (probably less than 30 ing/liter)
 Solubility in Organic*t  Soluble in  ether, benzene, and chloroform
 Log Octanol/Water  partition Coefficient}   4.93
 vapor Pressure!  Less than 0*1 an Hf at 25*C
 Vapor Density:   7.4
 Flash Point: 155*C
 Transport and Fate
      Much of the information concerning transport and fate
 is  inferred  from data for chlorinated benzenes in general because
 specific  information for 1,2,4,5-tetrachlorobeniene is lacking.
 Although  1,2,4,5-tetrachlorobenzene  has a relatively high boiling
 point and low vapor pressure, data for other chlorinated benzenes
 suggest that volatilization may be an important transport process
 1,2,4,5-Tetrachlorobenzene
 Oc1Sbe*r  1985
Preceding page blank

-------
 under  tone conditions.   The  lev  solubility and high  activity
 coefficient*  of  these compounds  in aqueous solution  nay account
 for their  unexpectedly  high  volatility.  Oxidation of  1,2,4,5-
 tetrachlorobenzene  in aquatic  systems  is unlikely.   However,
 soae photodegradation by hydroxyl radicals in the atmosphere
 nay occur. Photolysis  and hydrolysis  are unlikely environmental
 fates.

     The high log octanol/vater  partition coefficient  for 1,2,4,5-
 tetraehlorobenzene  suggests  that adsorption by organic soil
 particles  and by suspended and sedimentary organic materials
 in  aquatic environments is probably  an important environmental
 process.   It  is  also likely  that significant accumulation in
 the tissues of living organisms  occurs.  Although biodegradation
 may occur,  it probably  would proceed very slowly.


 Health Effects

     There are no reports of carcinogenic, teratogenic, or
 mutagenic  activity  by 1,2,4,5-tetrachlorobenzene in  humans
 or  experimental  organisms.

     Hats  receiving as  little  as 0.005 mg/kg/day orally for
 up  to  8 months are  reported  to show  a  disruption of  conditioned
 reflexes and  increased  liver weights*  Rabbits treated with
 0.05 mg/kg/day show liver glycogen-forming disorders after
 about  € months.  In beagles, administration of 5 mg/kg/day
 in  the diet is reported to cause a slight elevation  of serum
 alkaline phosphatase activity  and bilirubin levels after 24 months.
 In  this study, the  serum chemistry values returned to  normal
 within 3 months  after cessation  of exposure, and gross and
 histopathological changes conducted  20 months after  cessation
 of  exposure revealed no treatment related changes.   The oral
 LD.n values for  rats and mice  are 1,500 and 1,035 mg/kg, re-
 spectively.

     Tetrachlorobensenes appear  to induce microsomal enzymes
 and, therefore,  could increase the metabolism of compounds
 acted  on by the  cytochrome 9-430 system.  This could either
 increase or decrease the toxicity of the compound depending
 on  whether the metabolite was  more or  less active than the
 parent material.


 Toxicity to Domestic Animals and Wildlife

     An acute  value for 1,2,4,5-tetrachlorobenaene of  1,550 ug/liter
 is  reported for  the bluegill,  a  freshwater fish.  No freshwater
chronic values are  available.  The 96-hour BC..S for chlorophyll a
and cell numbers are 52,900  and  46,800 uf/litff, respectively for'
 the  freshwater alga Selenastrum  capricornuturn.  Among  saltwater
1,2,4,5-Tetrachlorobeniene
Page 2
October IfSS

-------
organisms, acute valuta fee ays id shrimp and the sheepshead
minnow art 1,480 and 840 yg/liter, respectively.  A chronic
value of 129 yg/lit«r and an acute-chronic ratio of 6.5 art
reported for the aheepshead minnow.  The 96-hour ECcgS for
chlorophyll a and cell numbers are 7,100 and 7,320 pf/liter,
respectively! foe the saltwater alga Sfceletoneaa costatua.

     The weighted average bioconcentration factor for 1,2,4,5-
tetrachlorobenzene and the edible portion of all freshwater
and estuarine aquatic organisms consumed by Americans is esti-
mated to be 1,125.


jegu1ations and 51andards

Ambient Hater Quality Criteria (USEPA):

     Aquatic Life

     The available data are not adequate for establishing criteria,

     Hunan Health

     Criterion:  38 Mi/liter


REFERENCES

AMERICAN CONFERENCE OP GOVERNMENTAL INDUSTRIAL HYGIENISTS (ACGXH).
     1980.  Documentation of the Threshold Limit Values.  4th ed.
     Cincinnati, Ohio.  108 pages

NATIONAL IHSTITOTE FOR OCOTPATIOHAI, SAFETY ASD HEALTI (HIOSH) .
     1984.  Registry of Toxic Effects of Chemical Substances.
     Data Base.  Washington, D.C.  April 1984

U.S. ENVIRONMENTAL PROTECTION AGENCY (USEPA).  1979.  Water-
     Related Environmental Fate of 129 Priority Pollutants.
     Washington, D.C.  December 1979.  EPA 440/4-79-029

U.S. ENVIRONMENTAL PROTECTION AGENCY (DSEPA).  1980.  Affblent
     Water Quality Criteria for Chlorinated Benzenes.   Office
     of Water Regulations and Standards, Criteria and Standards
     Division, Washington, D.C.  October 1980.  EPA 440/5-80-028

WEAST, R.E., ed.  1981."  Handbook of Chemistry and Physics.
     (2nd ed.  CRC Press, Cleveland, Ohio.  2,332 pages
1,2,4,S-Tetrachlorobenzene
f*f*. 3  _ _ _ _
October 1985

-------

-------
                          - i c.i/^rti_ni*vjnUU10 LNiU-p-
    Summary    ;

         Tetrachlorodibenzo-p-dioxin (TCDD) is often found as a
    contaminant in chlorinated phenolic compounds.  It persists
    in the natural environment and can be bioaccumulated.  Exposure
    to TCDD has been associated with numerous adverse health effects,
    including cancer, genotoxicity, enzyme induction, chloracne,
    teratogenicity, reproductive toxicity, imraunotoxicity, porphyria
    cut'anea tarda, and neurobehavioral changes.
    CAS Humbert   1746-01-6

    Chemical Formula:  C12H4C14°2

    10PAC Name;   2,3,7,8-Tetrachlorodibenzo-l,4-dioxin

    Important Synonyms and Trade Namesj  Dioxin, TCDD, 2,3,7,8-TCDD,
                                         2,3,7,8-tetrachiorodibenzo(b,e;
                                         (l,4)dloxin, tetradioxin



    Chemical and  Physical Properties

    Molecular weight;  321.9

    Boiling  Pointt   500*C (begins to decompose)
                    800*C (virtually complete degradation)

    Melting  Point:   302-305*C

    Solubility in Wateri   0.2 yg/liter at 20*C

    Solubility in Organics:  Soluble in fats, oils, and other rela-
                             tively nonpolar solvents
   Log Octanol/Kater Partition Coefficient!  5.16 (measured)

   vapor Pressure!   10~  aa Hg at 25*C

   Henry's Lav constants  2,"1 x 10"* ata a3 aol"*1
   TCDD
   Page  1
   October  1985
Preceding page blank
                                                     LClemcnc A»»ociat«a

-------
 Transport and fate

      2,3,7,S-Tetrachlorodibenzo-p-dioxin  (TCDD) has a *ery
 low vapor pressure and  therefore  is unlikely to volatixe into
 the atmosphere.   However,  there are studies that indicate volati-
 sation aay occur.  Experiments have shown TCDD to be highly
 sorbed to sediments,  soils, and biota so it nay be transported
 through the air  in soil dust*  Because TCDD is tightly bound
 to tolls, it is  probable that any surface water contaaination
 found in polluted areas is froa soil erosion rather than froa
 leaching.  A calculated sediment/water equilibrium partition    .
 coefficient using € sets of data  for TCDD varied from 1.1 x 10
 to 2.1 * 10'4.   This  indicates that most TCDD in water will
 be sorbed to particulates*

      TCDD does not readily undergo photodegradation unless
 solvents are present  that  will act as hydrogen donors during
 reductive dechlorination.  Certain aieroorganisaa have been
 found that will  degrade TCDD.  The half-life of TCDD in soil
 has been found to vary  froa 130 days to well over a year*
 Thus,  TCDD is persistent in the environaent.


 Health Effects

      A variety of health effects  have been associated or attri-
 buted to exposure to  very  low concentrations of TCDD in both
 experimental animals  and humans.  These effects include cancer,
 genotoxicity, ensyae  induction, teratogenicity and reproductive
 toxicity,  laaunotoxicity*  chloracne, porphyria cutanea tarda,
 and neurobehavioral toxicity.  TCDD has been shown to induce
 cancer in alee and rats following deraal or oral adainistration.
 Bpideaiological  studies on exposed populations provide suggestive,
 but not conclusive, evidence that TCDD is a carcinogen in humans.
 There is strong  evidence that TCDD is teratogenic to certain
 aniaal species,  however, the evidence on humans is weak.  Animal
 studies suggest  that  iaaunotoxieity is probably the most potent
 effect of  TCDD.   Both iaaunotoxieity and the enzyme inducing
 effect of  TCDD are probably mediated through a eytosolic receptor
with  high  affinity for  TCDD.  chloracne is the only clear effect
that TCDD  intoxication  has produced in humans.


Toxicity to Wildlife  and Domestic Animals

     Freshwater  aquatic species exposed to low concentrations
of. TCDD (in the  parts per^trillion range) for 4 days displayed
toxic  signs and  died  froa  40 to 140 days later.  Acute toxic
effects  were not  noted  in  many of the aquatic species' at the
level  of TCDD water solubility, 0.2 ug/litsr.  Horses exposed
to TCDD in  contaminated waste oil used to control dust in corrals,
became  sick and  died.
TCDD
Page 2
October 198S
                                   yz?

-------
Reg u 1 a 1 1 on s an d S t a n d a r d s

Ambient Water Quality Criteria  (USEPA) :

     Aquatic Life

     The available data are not adequate for establishing criteria
     However, EPA did report the lowest values known to be
     toxic in aquatic organisms.

     Freshwater

          Acute toxicity:  1.0 Hi/liter
          Chronic toxicity;  <0.001 ^g/ liter

     Saltwater

          Ho available data

     Human Health

     Estimates of the carcinogenic risks associated with lifetime
     exposure to various concentrations of TCDD in water are:

     Risk                             Concentration

     10~f                             .00013 ng/liter
       "
       *7
                                      .000013 ng/litar
     ID*                              .0000013 ng/liter

GAG Unit lisk  (USEPA) s  1.6xl05  (mg/kg/day)"1


REFERENCES

NATIONAL INSTITUTE FOR OCCUPATIONAL SAFETY AND HEALTH (NIOSH).
     1183.  Registry of Toxic Effects of Chemical Substances.
     Data Base.  Washington, B.C.  October 19S3

U.S. ENVIRONMENTAL PROTECTION AGENCY  (USEPA).  1971.  Hater-
     Related Environmental Fate of 129 Priority Pollutants.
     Vol. 1.  Washington, D.C.  December 1979.  EPA 440/4-79-029 .

O.S. ENVIRONMENTAL PROTECTION AGENCY  (OSEPA) .  1984.  Ambient
     Watte Quality Criteria for 2,3,7,8-Tetrachlorodibenzo-
     p-dioxin.  Office of Water Regulations and Standards,
     Criteria and Standards Division, Washington, D.C.  February
     1984.  EPA 440/5-840-007

VETERANS ADMINISTRATION (VA) .  19S1.  Review of Literature
     on Herbicides Including phenoxy Herbicides and Associated
     Dioxins.  Vols. 1 and 2t  Analysis of Literature.  Department
     of Medicine and Surgery, Washington, D.C.


TCDD

SctoJr 1985

-------
 U.S.  ENVIRONMENTAL  PROTECTION AGENCY  (USEPA).   1984.  Health
      Effects Assessaent  for  2,3,7,8-TCDD.  Environaental Criteria
      and Assessaent Office,  Cincinnati, Ohio.   September  1184.
      BCAO-CIM-H044   (Final Draft)

 U.S.  ENVIRONMENTAL  PROTECTION AGENCY  (USEPA).   1985.  Health
      Assessment Document for Dichloromethane  (Methylene Chloride),
      Office of Health  ani Environmental Assessment.  Washington,
      D.C.  February 1985.  EPA  600/8-82/004?

 VETERANS ADMINISTATION  (VA),  1984.  Review of  Literature  on
      Herbicides,  Including Phenoxy Herbicides and Associated
      Dioxins.  Vols. 3 and 4:   Analysis of Recent Literature
      on Health Effects.   Departnent of Medicine and Surgery,
      Washington,  D.C.
TCDD
Page 4
October 1983

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 Summary

      1,1,2,2-Tetrachloroethane  induces liver tumors when admin-
 istered  orally  to mice, and  it  was shown to be autagenic using
 microbial assays.  Upon administration to pregnant mice, it.
 reportedly had  embryotoxic effects and increased the incidence
 of malformations.  In experimental animals, acute and chronic
 exposure damages the liver/  central nervous system, and kidneys.
 In humans, acute exposure depresses the central nervous system
 and may  be fatal.  Chronic effects in humans include liver
 damage,  gastrointestinal disturbances* and effects on the central
 nervous  system.


 CAS numbers  79-34-5

 Chemical Formula:  C2S2C1>4

 IUPAC Kane:  1,1,2,2-Tetrachloroethane

 Important Synonyms and Txade Names:  sym-T*trachloroethane,
                                     acetylene tetrachlor ide,
                                     dichloro-2,2-dichloroethane


 Chemicaland Physical Properties

 Molecular Weight:  167.85

 Boiling  Point:  146.2'C

 Melting  Points  -36«C

 Specific Gravity:  1.5953 at 20*C

 Solubility in Water:  2,900  mg/liter at 20*C

 Solubility in Organics:  Soluble in alcohol* ether, acetone,
                         benzene* petroleum ether* carbon tetra-
                         chloride, chloroform* carbon disulfide,
                         dimethylformamide, and oils

 Log Octanol/Wattr Partition  Coefficient!  2.56
                       s
Vapor treasures  5 mm Hg at  2Q*C

Vapor Density:  5.79
1,1,2 ,2-Tetrachloroe thane
Page  1
October 1985

-------
 Transport  and  Fate
                 little  information  is  available  pertaining
 •pacifically to  the  environmental transport  and  fate of  1,1,2,2-
 tetrachloroe thane.   However,  predictions  concerning these pro-
 cesses  can be aade based on comparison with  similar compounds
 such as 1,1,1-trichloroethane.  Photolysis and oxidation do
 not appear to be significant  aquatic fate processes for  1,1,2,2-
 tetraehloroe thane.   However,  based  on analogy with 1,1,1-tri-
 chloroethane,  stratospheric photodissociation by high energy
 ultraviolet light,, and tropospheric  photooxidation via reaction
 with hydroxyl radicals  seea likely  to be  relatively iaportant
 fates.   No information  related  specifically  to hydrolysis of
 1,1 ,2 ,2-tetrachloroethane  in  the environment is  available.
 However,  the low observed  reactivity of 1,1,1-trichloroethane
 suggests  that  hydrolysis of 1,1,2, 2-tetrachloroethane would
 occur too slowly to  be  an  iaportant fate  process.  Available
 data indicate  that relatively rapid volatilization of 1,1,2,2-
 tetrachloroe thane from  surface  waters can occur.  Thus,  although
 some of this compound will be absorbed froa  the atmosphere
 by  surface water and return to  earth in precipitation, atmos-
 pheric  photooxidation and photodissociation  are probably the
 most important environmental  fates.

     Based  on  analogy with 1,1,1-trichloroethane, sorption
 of  1,1,2,2-tetrachloroethane  to clay . sediments probably  is
 not an  iaportant process.  The  log  octanol/water partition
 coefficient of 2.56  for this  compound indicates  that sorption
 by  organic  particulars and bioaccuaulation may  occur to some
 extent; however,  no  adequate  empirical data, are  available.
 Available  inforaation concerning related compounds suggests
 that biotransformation  and blodegradation occur at low rates
 or  not  at  all.
Health. Effects

     1,1,2,2-Tetrachloroethane is a liver carcinogen whan admin-
istered orally to mice.  IARC concludes that there is limited
evidence for it* carcinogenicity in experimental animals.
This compound is autagenic in at least two bacterial tester
strain*.  Administration of 300*400 ag/kg/day to aice during
organogenesis is reported to produce embryo toxic effects and
slightly increase the Incidence of aalforaations.
                         \
     1,1,2,2-Tetrachloroethane produces acute and chronic toxic
effects in laboratory animals exposed by various routes.  Toxic
act don is primarily on the liver.  However, effect* on the
central nervous system, kidneys, and other tissues are also
reported; and acute exposure can be fatal*  The oral LD-n in
rats is 250 ag/kf.                                     9U


1,1,2,2-Tetrachloroethane
Page 2
October 1985

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     Numerous  deaths  in humans  have  been  reported,  primarily
as a result of occupational exposure by ingestion,  inhalation,
of skin contact.  Acute exposure  produces  central nervous  system
depression.  Chronic  effects  include hepatotoxicity and gastro-
intestinal disturbances in addition  to central nervous system
effects such •« tremors, dizziness,  headache, paralysis, and
polyneuritis.


Toxicity to Wildlife  and Domes tie^ AnJIM Is

     Acute values for freshwater  species  range from 9,320  ug/liter
for an invertebrate species to  approximately 20,000 ug/liter
for two species of fish.  An  embryo-larval  test conducted  with
the fathead minnow provides a chronic value of 2,400  pg/liter
and an acute-chronic  ratio of 8.5 for this  species.   Among
saltwater species* acute values of 9,020  ug/liter for the  nysid
shrimp and 12,300 M9/liter for  the sheepshead minnow  are reported.
Exposure to 1,1,2,2-tetrachloroethane affects chlorophyll  a
and cell numbers of algae exposed to approximately  141*000 ug/lite:
in a freshwater species and 6,300 ug/liter  in a saltwater  species.
TJ5e weighted average  bioconcentration factor for the  edible
portion of all freshwater and estuarine aquatic organisms  con-
sumed by Americans is 5.0.


Regulations and Standards

Ambient Water Quality Criteria  (OSEPA) :

     Aquatic Life

     The available data.are not adequate  for establishing  criteria.

     Hunan Health

     Estimates of the carcinogenic risks  associated with lifetime
     exposure to various concentrations of  1,1,2,2-tetrachloro-
     ethane in water  are:

                                        Concentration
                                        1.7 ug/littr
                                        0.17 ug/littr
                                        0.017 uf/liter
                                       -1
CAG Unit, Risk  (DSSPA) :  0.2  (mg/kg/dayi
HIOSH Recommended Sjtandardz  7 mg/m  TWA

OSHA Standard (skin)i  35 »g/m3
1,1,2,2-Tetrachloro«thane
Page 3
October 1985
                                                 [Ci»m«nt A«8ocia

-------
                       values  isfcin):   7 ag/aJ,TWA
                                       35 ag/n'* STEL
 REFERENCES
 AMERICAN  CONFERENCE Of GOVERlttENTAL  INDUSTRIAL BYGIBNISTS  (ACGIH)
      1980.  Documentation of  the Threshold Limit Values.   4th
      ed.  Cincinnati, Ohio.   48S
 INTERNATIONAL AGENCY FOR RESEARCH ON CANCER  (IARC).  1979.
      IARC Monographs on the Evaluation of Carcinogenic Risk
      of  Chemicals  to Humans.  Vol. 20 1  Some Halogenated Hydro-
      carbons.  World Health^ Organization, Lyon, France.  Pp.
      477-4S9

 NATIONAL CANCER  INSTITUTE  (NCI).  1978.  Bioassay of 1,1,2,2-
      Te t rachl or oe thane for Possible Carcinogenicity.   (CAS
      No. 79-34-5)  NCI Carcinogenesis Technical Report Series
      No. 27.  Washington, D.C.  DH2W Publication No. (Nil}
      78-827

 NATIONAL INSTITUTE FOR OCCUPATIONAL SAFETY AND HEALTH  (NIOSH) .
      1976.  Criteria for a Recommended Standard— Occupational
      Exposure to 1,1,2 ,2-Tetrachloroe thane.  Washington/ D.C.
      DflEW Publication No.  (NIOSH) 77-121

 NATIONAL INSTITUTE FOR OCCUPATIONAL SAFETY AND HEALTH  (NIOSH \ .
      1984.  Registry of Toxic Effects of Chemical Substances.
      Data. Base.  Washington, D.C.  October 19S4

 SAX,  N.I.  1975.   Dangerous Properties of Industrial Materials.
      4th ed.  Van  Nostrand Reinhold Co., New York.  1,258 pages

 U.S.  ENVIRONMENTAL PROTECTION AGENCY (USEPA) .  1979.  Water-
      Related Environmental Fate of 129 Priority Pollutants.
      Washington, D.C.  December 1979.  SPA 440/4-79-029

 U.S.  ENVIRONMENTAL PROTECTION AGENCY (OSEPA).  1980.  Ambient
      Water Quality Criteria for Chlorinated Ethanes.  Office
      of Water Regulations and Standards, Criteria end Standards
      Division, Washington, D.C.  October 1980.  EPA 440/5-80-029

 U.S.  ENVIRONMENTAL PROTECTION AGENCY (USEPA}.  1984.  Health
      Effects Assessment for 1, 1,2,2-Tetrachloroethane.   Final
      Draft.  Environmental Criteria and Assessment Office,
      Cincinnati, Ohio.  v September 1984.  SCAO-CIH-H032

U.S.  ENVIRONMENTAL PROTECTION AGENCY {OSEPA),  1985.  .Health
      Assessment Document for Dichloroamthane (Metbylene Chloride)
      Office of Health and Environmental Assessment, Washington,
      D.C.  February 1985.  SPA 600/8-82/004F


 1, 1,2,2-Tetrachloroethane
Page  4
October  1985

-------
 WEASf,  R.E., ed.   1981.  Handbook of Chemistry and  Physics
      62nd ed.  CRC Press, Cleveland, Ohio.   2,332
1,1,2,2-Tetrachloroethane
P»9« 5
October 1985

-------

-------
                        TETRACHLOROETHYLB1E
 Summary
      Tetrachloroethylene (PCE, perchloroethylene) induced liver
 tumors vh*n administered orally to mice and *»« found to be
 mutagenic using a microbial assay system.  Reproduction toxicity
 was observed In pregnant rats and alee exposed to high concentra-
 tions.  Animals exposed by Inhalation to tetraehloroethylene
 exhibited liver/ kidney, and central nervous system damage.
 CAS Number:  127-18-4
 Chemical Formula:  C2C14
 IUPAC Mame:  Tetrachloroethene
 Important Synonyms and Trade Names:  Perchloroethylene,  PCE
 Chemical and Physical Properties
 Molecular Weight:  165.83
 Boiling Points   121»C
 Melting Point:   -22.7»C
 Specific Gravity:  1.63
 Solubility in Water:   150 to 200 ng/littr at 20*C
 Solubility in Organicsi  Soluble in alcohol, ether* and  benzene
 Log Octanol/Water Partition Coefficients  2.88
 Vapor Pressure:  14 an Ig at 20*C
 Transport and Fate
      Tetracbloroethylene (PCE) rapidly volatiziles into the
 atmosphere where it reacts with bydroxyl radicals to produce
 HC1, CO, CO. and carboxyllc acid.  This is probably the most
 important transport and fate process for tetrachlorbethylene
 in the environment.  PCE will leach into the ground water, espe-
 cially in soils of low organic content.  In soils with high
 levels of organics, PCE adsorbs to these, materials and can
 Tetrachloroethylene
 page 1
 October 1985
Preceding page blank

-------
 be bi©accumulated  to 10111*  degree.   However,  it. if  unclear  if
 tetrachloroethylene  bound  to  organic  material  can  be  degraded
 by microorganisms  or must  be  desorbed to be  destroyed.  There
 is some  evidence that higher  organisms can metabolize PCS,


 Health Effects

     Tetrachloroethylene was  found  to produce  liver cancer
 in aale  and  female alee when  administered  orally by gavage
 (NCI 1977).   Unpublished gavage  studies in rats and nice per-
 formed by  the national Toxicology Program  (NT?) showed  hepato-
 cellular carcinomas  in mice and  a slight,  statistically insig-
 nificant increase  in a rare type of kidney tumor.   NT? is
 also conducting an inhalation carcinogenicity  study.  Elevated
 autagenic  activity was found  in  Salmonella strains treated
 with tetrachloroethylene.  Delayed  ossification of skull bones
 and sternebrae were  reported  in  offspring  of pregnant aice
 exposed  to 2,000 mg/m of  tetrachloroethylene  for 7 hours/day.
 on days  6-15  of gestation.  Increased fetal  resorption* were
 observed after exposure of pregnant rats to  tetrachloroethylene.
 Renal toxicity and hepatotoxicity have been  noted following
 chronic  inhalation exposure of rats to tetrachloroethylene
 levels of  1,356 mg/m .  During the  first 2 weeks of a subchronic
 inhalation study/  exposure to concentrations of 1,622 ppm
 {10,867  mg/m  ) of  tetrachloroethylene produced sign*  of central
 nervous  system depression, and cholinergic stimulation  was
 observed among rabbits, monkeys, rats,  and guinea pigs.


 Toxicity to Wildlife  and Domestic Animals

     Tetrachloroethylene is the  most  toxic of  the chloroethylenes
 to aquatic organisms  but is only moderately  toxic relative
 to other types of  compounds.  The limited  acute toxicity data
 indicate that the  LC.- value  for saltwater and freshwater species
 are similar,  around  10,000 pg/litert  the trout was the  most
 sensitive  (LC-- •  4,800 ug/littr).  Chronic  values were 840
 and 450  ug/lillr for  freshwater  and saltwater  species,  respec-
 tively,  and an acute-chronic  ratio  of II was calculated.

     No  information on the toxicity of tetrachloroethylene
 to terrestrial wildlife or domestic animals  was available in
 the literature reviewed.
  . Mennear, NTP Chemical Manager; personal communication, 1984
Tetrachloroethylene
Page 2
October IS85

-------
 Regulations  and Standard!

 Ambient Water Quality Criteria  (USEPA)i
        '
      Aquatic Life

      The  available data, are not adequate for establishing criteri
      However, EPA did report the lowest values known to be
      toxic to aquatic organisms.

      Freshwater

          Acute toxicity:  5,280 ug/liter
          Chronic toxicityi  840 M9/liter

      Saltwater

          Acute toxicity:  10,200 uf/liter
          Chronic toxicity:  450 M9/liter

      Hunan Health

      Estimates of the carcinogenic risks associated with lifetime
      exposure to various concentrations of tetrachloroethylene
      in water are:


      Risk                        Concentration

      I0l!                        i.O ug/liter
      10 :                        0.8 jig/liter
      10"'                        0.08 M9/lit»r


 CAG Onit Risk (OSEPA)5  S.lxlfl"2 (nf/ki/dayj*1

 NIOSH Recommended Standards (air)s  335 ag/al TWA
                                    €70 ag/ar 15-min Ceiling Level

 OSHA  Standards (air):   670 mg/m3 TWA
                        1,340 ag/al Ceiling Level
                        2,010 mg/m  for S min every 3 hr, Peak Leve]


 RSFfREMCES

 NATIONAL ACASBIC OF  SCIENCE (HAS).  1977.  Drinking Mater and
     Health.  Safe Drinking Mater Committee/ Washington, D.C.

 NATIONAL CANCER INSTITUTE  (NCI).  1977.  Bioassay of Tetrachloro-
     ethylene for Possible Carcinogenicity.  NCI Carcinogene-sis
     Technical Report Series No. 13, Washington, D.C.  DHEW
     Publication No. (NIB) 77*813
Tetrachloroethylene
Page 3
October 1985

-------
 NATIONAL INSTITUTE FOR OCCUPATIONAL SAFETY AND HEALTH  (NIC
      19S3.   Registry of Tdxle Effects of Chemical Substanc
      Data. Base.   Washington,  D.C.   October 1983

 U.S.  ENVIRONMENTAL PROTECTION AGENCY (OStPA) .   1179.   Bea.'
      Assessment  Document for  Tetrachloroethylene (Perchlor
      tn«).   External Review Draft  No, 1, April 1979

 0.5.  ENVIRONMENTAL PROTECTION AGENCY (USEPA).   1979.   Wate
      Related Environmental  fat* of 129 Priority Pollutants
      Washington, D.C.  December 1979.  EPA 440/4-79*029

 U.S.  ENVIRONMENTAL PROTECTION AGENCY (USEPA).   1980.   Aabi
      Wattr  Quality Criteria foe Tetrachloroethylene.   Offi
      of  Wattr Regulation! and Standards, Criteria and  Stan
      Division, Washington,  D.C.* October 1980.  SPA 440/5-

 U.S.  ENVIRONMENTAL PROTECTION AGZHCY (DSZPA).   1984.   Heal
      Effects A»»estment for Tetrachloroethylene.   Final  Dr.
      Environnental Criteria and Assessment Office, Cincinn,
      Ohio.   September 1984.  ECAO-CIN-E009

 U.S.  ENVIRONMENTAL PROTECTION AGENCY (USEPA}.   1985.   leal'
      Assessment  Document for  Chloroform*  Office of Health.
      and Environmental Assessment,  Washington, D.C.  Scoter
      1985.   EPA  600/8-84/004F

 VERSCHUEREN,  K.   1977.   Handbook of Environmental Data, on c
      Chemicals.   Van Sostrand Reinhold Co., New York.  659

 WEAST", R.E.,  ed.   1981.   Handbook  of Chemistry and Physics.
      62nd ed.  CRC Press, Cleveland,  Ohio.  2,332 pages
Tetraehloroe thy lane
Page 4
October 1985

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                         TETRAETHYL LEAD
Summary
     Tttraethyl lead  (TEL) is likely to have adverse effects
on human reproduction and embryonic development.  Human exposure
Has been associated with adverse effects on the central nervous
system, peripheral nerves, kidneys, and henatopoietic system.
CAS Number i  78-00-2
Chemical Formulas   (C2Hj)
I UP AC Kane i  Tetraethyl lead
Important Synonyms  and Trade Names:  Tetraethyl plumbane, TEL

Chemical and Physical Properties
Molecular Height:   323.45
Boiling Points  Approximately 200 *C
Melting Polnti  -13f.8*C
Specific Gravity!   1.653 at 20*C
Solubility In Water t  Insoluble
Solubility in Organic* i  Soluble in most organic solvents
Vapor Pressuret  1 ma Hg at 38.4*C
Plash Points
Transport and Fate
     Volatilization of tetraethyl lead  tTBL) from aquatic or
terrestrial systeas may be a significant transport process.
However, its presence in" the atmosphere probably would be transi-
ent, because photochemical decomposition occurs readily.  The
organic and inorganic Itad compounds formed can then be removed
from the atmosphere by wet or dry deposition.
     Sorption processes in sediments and soils nay be important
for TEL.  However, TEL is generally not stable in aerobic environ-
Tetraethyl lead
Page 1
October 1985

-------
aents.   TIL decomposes slowly at room temperature and more
rapidly  at elevated  temperatures.  In aquatic systems, a signifi-
cant  portion of TEL  is probably oxidized in the water column.
Overall, nost TEL probably undergoes conversion to inorganic
lead  compounds relatively quickly.  The types of compounds
formed and their subsequent environmental fates ace determined
by  local physical and chemical conditions.


Health Effects
    •7.- •
    *  There are no reports of carcinogeniclty, mutagenicity,
or  teratogenicity in humans as a result of exposure to TIL.
Young female Swiss sice developed malignant lynphomas after
subcutaneous exposure to TEL.  However, the significance of
these findings could not be evaluated because of the low tunor
incidence in only one sex and because the type of tumor observed
occurs spontaneously and with variable Incidence in the strain
of  mouse studied.  Although specific results with TEL are not
available, lead is reported to have adverse effects on human
reproduction and embryonic, fetal, and postnatal development.
fetotoxicity and postimplantatlpn mortality are reported to
occur after oral administration to pregnant cats.

      TEL is toxic to humans and experimental animals by oral,
inhalation, and cutaneous routes of exposure.  Effects are
commonly seen, in the central nervous system, peripheral nerves,
the kidney, and hematopoletic system.  In humans, TEL intoxica-
tion  is reportedly characterized by insomnia, hallucinations,
emotional Instability, and increased physical activity of an
erratic nature.  After exposure to high concentrations', coma
and death may occur.  An oral L&.Q value of 17 mg/kg and
an  Inhalation LC.O value of 850 mg/m  for €0 minutes are
reported for the cat.  Lethal dermal doses of 547 mg/kg and
830 mg/kg are reported for the dog and rabbit, respectively.


Toxleity to Wildlife and Pomestic Animals

     Although lead is known to occur in the tissues of many
free-living wild animals, including birds, mammals, fishes,
and invertebrates, reports of poisoning usually involve waterfowl
that  Ingest lead shot.  There also is evidence that lead, at
concentrations occasionally found neac roadsides and smelters,
can eliminate or reduce populations of bacteria and fungi on
leaf surfaces and in soil.  Cases of lead poisoning have been
reported foe a variety of domestic animals, including cattle,
horses, dogs, and cats.  It is probable that poisoning in wild-
life and domestic animals involves exposure to elemental lead
or lead compounds other thaa TEL.  One study reports an EC50
value of 150 ug/litec la a saltwater alga exposed to TEL.
Tetraethyl lead
Page 2
October 1985

-------
Regulations and Standards

NIOSH Recommended Standard:  0.10 mg/m3 TWA  (as Pb)

OSHA Standardi  0.075 mg/m3  (as Pb)

ACGIH Threshold Limit Values:  0.1 mg/m3 TWA  (ai Pb)
                               0.3 mg/nr STEL  (as Pb)


REFERENCES

AMERICAN CONFERENCE OF GOVERNMENTAL INDUSTRIAL HYGIENISTS  (ACGIH).
     1980.  Documentation of the Threshold Limit Values.   4th
     ed.  Cincinnati, Ohio.  488 pages

DOULL, J., RLAASSEN, L.D., and AMDOR, M.O.» eds,  1980.  Casarett
     and Doull's Toxicology:  The Basic Science of Poisons.
     2nd ed.  Hacnillan Publishing Co.* New York.  778 pages

INTERNATIONAL AGENCY FOR RESEARCH ON CANCER  (IARC).  1973.
     IARC Monographs on the  Evaluation of Carcinogenic Risk
     of Chemicals to Man.  Vol. 2:  Some Inorganic and Organo-
     aetallic Compounds.  World Health Organization, Lyon,
     France.  Pp. ISO-ISO

INTERNATIONAL AGENCY FOR RESEARCH ON CANCER  fIARCJ.  1980.
     IARC Monographs on the  Evaluation of Carcinogenic Risk
     of Chemicals to Bunans.  Vol. 23:  Seat Mttals and Metallic
     Compounds.  World Health Organization, Lyon, Prance.
     fp. 325-341

NATIONAL ACADEMY OF SCIENCES (NAS).  1972.  Lead:  Airborne
     Lead in Perspective.  National Academy Press, Washington,
     D.C.  330 pages

NATIONAL INSTITUTE FOR OCCUPATIONAL SAFETY AND HEALTH (NIOSH),
     1984.  Registry of Toxic Effects of Chemical Substances.
     Data Base.  Washington, D.C.

SAX, N.I.  1975.  Dangerous Properties of Industrial Materials.
     4th ed.  Van Nostrand Reinhold Co., New fork.  1,258 pages

O.S. ENVIRONMENTAL PROTECTION AGENCY (USEPA).  1979.  Water-
     Related Environmental Fate of 129 Priority Pollutants.
     Washington, D.C.  December 1979.  EPA 440/4-79-029
                        v
U.S. ENVIRONMENTAL PROTECTION AGENCY CUS1PA).  1983.  Air Quality
     Criteria for Lead (Review Draft).  Office of Research
     and Development, Washington, D.C.  October 1983.  EPA-600/8-83-02
Tetraethyl Itad

        1985
                          £03

-------
O.S. ENVIRONMENTAL PROTECTION AGENCY  (USEPA).  1913.  Revis
     Section • of Aabitnt watte Quality Criteria for L«ad.
     Draft R*port.  Offiet of Water Regulations and standar
     Crittria and Standards Division, Washington, D.C.  Auq
     19S3                                                 J
Tttratthyl l«ad
Pag« 4
October 1985

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                         TETHAHYDROPUBAN
Summary
     Tetrahydrofuran was found to be mutagenie using a microbial
assay system and caused chromosomal aberrations In Chinese
Hamster Ovary Cells.  Technical tetrahydrofuran has been shown
to  irritate the skin and cause liver and kidney damage.


CAS Number:  109-99*9

Chemical Formula:  CjH.O

IDPAC Name:  Tetrahydrofuran

Important Synonyms and Trade Names:  Diethylene oxide, butylene
                                     oxide, tetramethylene oxide,
                                     hydrofuran, THF


Chemical and PhysicalProperties

Molecular Weight:  72.12

Boiling Point?  67*C

Melting Points  -65«C

Specific Gravity:  0.8892 at 20«C

Solubility in Water:  Soluble in water

Solubility in Organics:  Very soluble in alcohol, ether, acetone,
                         benzene, and other organic solvents

Vapor Pressure:  143 mm Bg at 20*C

Vapor Densityi  2.S


Transport and Fate

     Little information is available on the transport and fate
of tetrahydrofuran in the natural environment,  it has a rela-
tively high vapor pressure and should therefore volatilize into
the atmosphere.  Upon exposure to ultraviolet radiation, it
produces ozone, aldehydes, and epoxides and apparently is not
very persistent.  In aquatic systems, its volatilization would
be somewhat limited by its rather high water solubility.  Its
water solubility also suggests that tetrahydrofuran probably


Tetrahydrofuran
Page 1
October 19S5
                                                  Clement Associates

-------
moves readily through soil and Is not bioaceumulated to any
substantial degree.


Health Effects

     Tetrahydrofuran is currently being tested by the nation
Toxicology Program to assess Its carcinogenic potential.  No
evidence of carcinogenic, reproductive, or teratogenic effec
associated with exposure to tetrahydrofuran vas found in the
literature reviewed.  It was found to be nutagenie in a mic:
assay on Eseheriehia eeli and caused chromosomal aberrations
but not sister chromatedexchange in Chinese hamster ovary
cells.

     Exposure to 590 mg/n* tetrahydrofuran for 6 hours/day
caused decreased pulse pressure in dogs after 4 weeks, but
no histopathological changes occurred In aajor organs after
12 weeks.  Dally (oral?) administration of 20 mg/kg for 6 mo;
caused weight loss, paralysis of the hind limbs, hyperemia
of the viscera and protein dystrophy of the liver (Pozdnyako1
in 1SEPA 1980).  Pure tetrahydrofuran does not appear to cau<
toxic effects even at very high concentrations (greater than
lOtOOO g/m ), but the technical compound, which is contaninat
with peroxidesf causes skin irritation and liver and kidney
damage.  The oral LD5Q in rats vas reported to be 2,800 ag/kc


Toxieity to Wildlife and Domestic Animals

     Ho information on the toxicity of tetrahydrofuran to \
life and domestic aniaals was available in the literature rev
Regulations and Standards

OSHA Standard  (air) t  590 ag/a3 TWA

ACGtH Threshold Liait Values:  590 mg/m? Tim
                               735 ttf/a  STEL


HBF8R2HC8S

AMERICAN COOHCIL OF COVESKIIENTAL IHOCST1IAI, HYCSIINISTS  (ACGIH
     1980.  Docuaentation of the Threshold Limit values.  4th
     ed,  Cincinnati, Ohio.  401 pages

1WTJOWAL IHSTIT0T! FOR OCCOPATIOHJU, SAFETY AND HEALTH  (NIOSH5
     1984.  Xeglstry of Toxic Effects of Cheaical Substances.
     Data Base.  Washington, D.C.  July 1984
Tetrahydrofuran
Page 2
October 1985

-------
NATIONAL TOXICOLOGY PROGRAM  (RTF).  1984.  Fiscal Year 1984
     Annual flan.  February  1984.  OSDHHS.  NTP-84-Q23

U.S. ENVIRONMENTAL PROTECTION AGENCY  (USEPA).  1980.  TSCA Chemical
     Assessment Series—Chemical Hazard Information Profiles
      (CHIPs).  Office of Pesticides and Toxic Substances.
     Washington, D.C.  April 1980.  OSEPA 560/11-80-011

VERSCHUEREN, X.  1977.  Handbook of Environmental Data on Organic
     Chemicals.  Van Nostrand Reinhold Co., New York.  659 pages

WZAST, R.E., ed.  1981.  Handbook of Chemistry and Physics.
     62nd ed.  CRC Press, Cleveland, Ohio.  2,332 pages
Tetrahydrofuran
Page 3
October 1985

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                             THALLIUM
Summary

     Acute exposure to soluble thallium compounds has been
associated in humans with gastrointestinal irritation; damage
of the liver, kidneys, and central and peripheral nervous sys-
tems; pulmonary edema; degenerative changes in the adrenals;
and-'ocular effects.
CAS Number:  7440*28-0

Chemical Formulat  Tl

IUPAC Mane;  Thallium


Chenical and phyaical properties

Atonic Weight:  204.37

Boiling Pointt  1,457«C

Melting Pointi  303.S*C

Specific Gravity;  11.85

Solubility in Wateri  Insoluble  (many confounds are soluble)


Transport and Fate

     In reducing environments, thallium may be precipitated
as the metal or as thallium sulfide.  However, much of the
thallium present in aquatic systems is likely to remain in
solution and be transported to the oceans.  Active removal
of sone dissolved thallium by sorption to clay minerals and
hydrous metal oxides present in bed sediments is probably an
important environmental fate process'.  Thallium is readily
taken up by aquatic organisms, and bioaccumulation may also
be an important fate process.  Results of liaited studies with
algae suggest that thallium nay also be available for food
chain magnification*  There is no evidence to suggest that
photolysis or volatilization are important environmental pro-
cesses.  Although there is speculation that thallium can be
methylated under aerobic conditions by electrophilic attack,
biotransforaation does not appear to be an important process
in aquatic systems.


Thallium
Page 1
October 1981
       Preceding page Wank

-------
 Health Effects

      There is no evidence  that thalliua  is carcinogenic in
 human* of  experimental  aniaals,  and  it does not  appear  to have
 •ignificant autagenic activity.   Exposure  to thalliua salts
 during critical developmental  stages ia  repotted to  product
 achondioplaaia ia chickens and rats. Ho other significant
 teratogenic effects act reported.

      Thallium, in th* form of  soluble compounds, is  readily
 absorbed  through the skin  and  gastrointestinal tract.   Symptoms
 associated wi-th acute poisoning  in humans  include gastrointestinal
 irritation;  liver and kidney damage;  pulmonary edema; degenerative
 changes in the adrenals* peripheral  nervous system,  and central
 nervous systemf and ocular effects*  including optic  neuritis
 and,  rarely,  cataracts. The estimated lethal dose for  humans
 is  8  to 12 ag/kg.  In experimental animals, thallium compounds
 produce effects similar to those seen in humans.  Rats  appear
 to  be particularly sensitive to  the  cataractogenic activity
 of  thalliua.   Regardless of the  specific thallium compound
 tested, rate  of intake, 01 rout* of  adainistration,  LD.Q values
 for a variety of species range from  about  3 to 92 ag/kfl


 Toxiclty to Wildlife and Domestic Animals

      Acute and chronic  toxicity  of thalliua to freshwater aquatic
 life  occurs at concentrations  as low as  1,400 and 40 Mg/liter,
 respectively.   Acute toxicity  to saltwater aquatic life occurs
 at  concentrations as low as 2,130 ug/liter. Toxic effects
 would be expected to occur at  lower  concentrations among species
 •ore  sensitive than those  tested,  Bioconcentration  factors
 ranged. from about 11 for the mussel  Mytilus edulis to about
 1.5x10 for other freshwater and aar ine  inver t ebr a t es .   values
 of  about 1x10   are reported for  marine and freshwater fish.


 Regulations and Standards

 Ambient Water  Quality Criteria (tJSEPA) i

      Aquatic Life

      Th* available data ar* not  adequate foe establishing criteria,

      Human Health
                           \
      Criterion!   13 jig/liter

 OSHA  standard!   100 ug/a3
ACGIH Threshold Level Value:  0.1 mg/a3 TWA  (soluble  compounds,
                              as Tl)
Thalliua
Page 2
Octob*r 1985

-------
 REFERENCES

 AMERICAN CONFERENCE OF GOVERNMENTAL  INDUSTRIAL BYGIENXSTS  (ACGIH)
      1980.  Documentation of the Thrtshold Limit Valuta.   4th.ed.
      Cincinnati! Ohio.   488 page*

 DOOLL, J.» KLAASSEH, C.D., and AMDUR, M.O.  1980.  Casarett
      and Doull'i Toxicology:  The Basic Science of Poisons.
      2nd «d.  Macmillan  Publishing Co., New York.  778 pages

 NATIONAL INSTITUTE FOR OCCUPATIONAL  SAFETY AND HEALTH  (NIOSH).
      1984.  Registry of  Toxic Efftct* of Chemical Substances.
      Data Baa*.  Washington, D.C.  July 1984

 SHEPARD, T.B.  1980.  Catalog of Teratogenic Agents.  3rd  ed.
      Johns Hopkins University Press, Baltimore.  410 pages

 0.5.  ENVIRONMENTAL PROTECTION AGENCY (DSEPA).  1979.  Water-
      Related Environmental Fate of 129 Priority Pollutants.
      Washington, D.C.  December 1979.  EPA 440/4-79-029

 D.S.  ENVIRONMENTAL PROTECTION AGENCY (USEPA).  1980.  Ambient
      water Quality Criteria for Thallium.  Office of Water
      Regulations and Standards, Criteria and Standards Division,
      Washington, D.C.  October 1980.  EPA 440/5-80

 WEAST, R.E., ed.  1981.  Handbook of Chemistry and Physics.
      62nd ed.  CRC Press, Cleveland, Ohio.  2,332 pages
Thallium
Pag* 3
October 1985

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                              TITANIUM
    -~ Titaniua dioxide produced injection-site  tuaors in rats
 given intramuscular injection* and lung tuaors in- rats  exposed
 by inhalation.  In humans, inhalation exposure to high  concen-
 trations of titanium dioxide has caused slight fibrosis of
 the lung.
 Background Information  '  "         '...--.

      Titanium is the ninth aost abundant aleaent  in the  crust
 of the earth and is alaost always present  in  igneous rocks
 and in the sediments derived froa tbea.  Titanium is an  active
 metal, but it resists decomposition because of  the formation
 of a protective titanium dioxide fila.  The fila  is insoluble,
 repairable, and provides excellent corrosion  resistance.  Conse-
 quently, titanium resists corrosion in all naturally occurring
 environments, including air, soil* and water.

 CAS number»  7440-32-6  : --  ?i"*   "c  "r-"v-

 Chemical Formula*  Ti       ,...._._  ....:,  7;-..._.-. =_.;',.. .;-   ,.•--••_..;

 IOTAC Name:  Titaniua         _  	   ,            -
 Chemical and Physical Properties

 Atomic Weight?  47.§0
                                 •  . .   • . •- «  >• "   ' • •     ""' .
 lolling foint?  3,2S?*C       :-""~

 Melting Point?  1,660«C         :_ ^     :    "",

 Specific Sravityt  4.5

 Solubility in Wateri  Insoluble                       :


 Transport and Fate '^- '••^'" '••j:-^-f~*°  ~*~ *'_ ^.\;..,^  "'':- .

      Host common titanium compounds are  insoluble In water
 and  partitioning of auch of the titanium in aquatic  systems
 into the bottom sediments would be expected.  Atmospheric trans-
 port of titanium, and subsequent wet and dry deposition, can
 occur."   •   -   	- ••-••-  • --•' '- • •'•	"
Titaniua
page  1
October 1985
Preceding page blank

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Health Effects

     Thtrt  is no  evidence  to  suggest  that  titanium  is  carcino-
genic in humans.  Titanium dioxide  is reported to have tumori-
genic effects at  the  site  of  intramuscular  Injection in rats.
Preliainary results of  a 2-year B.I. Dupont (1983)  study show
increased incidences  of squamous cell carcinoma of  the lung
and  bronchioalveolar  adenoma  in rats exposed to airborne con-
centrations of  250 mg/sr of titanium dioxide.  Results of a
2-year feeding  study  conducted for  the National Cancer Institute
indicated that  titanium dioxide was not carcinogenic in rats
and  mice under  the conditions of the bioassay.  There  are no
reports of  mutagenie, tcratogenic, or reproductive  effects
associated  with exposure to titanium  in humans or experimental
animals.

     In humans, most  of the body burden of  titanium is in the
lungs.  About one-third of inhaled  titanium is thought to 'be
retained in the lungs.  Slight fibrosis has been observed after
inhalation  exposure to  high concentrations  of titanium dioxide
dust.  However, titanium generally acts as  an inert particulate
material in the lungs.  Titanium does not appear to produce
significant skin  irritation or to cause toxic effects  after
ingestion in humans or  experimental animals.


Toxicity to Wildlife  and Domestic Animals

     The available data are not adequate to characterize the
toxieity of titianium to wildlife and domestic animals.


Regulations and Standards

ACGIH Threshold Limit Values:

     10 mg/m| TWA (titanium dioxide, total  dust)
      5 mg/mf TWA (titanium dioxide, respirable dust}
     20 mg/mj STEL (titanium dioxide)


REFERENCES

AMERICAN CONFERENCE OF  GOVERNMENTAL INDUSTRIAL HYGIENISTS (ACGIH).
     1980.  Documentation  of the Threshold  Limit Values.  4th ed.
     Cincinnati, Ohio.  488 pages

DOOLL, J.,  KLAASSEN,  C.D., and AMDUR, N.O.  1S80.   Casarctt
     and Doull's Toxicology:  The Basic Science of  Poisons.
     2nd ed.  Macmillan Publishing Co., Hew York.   778 pages
Titanium
fage 2
October 1985

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      .......  _, 		  	   1983.  Letter  to Document
      Control Officer  (WI  557), Chemical Information Division,
      Office  of Toxic  Substances, O.S. Environmental Protection
      Agency.  TSCA Section  8(e) Submission file 8IKQ-1083-04S7.
      October 17, 1983

INITTEL, 0.  1983.  Titanium and titaniua alloys.  In lirk-Othmer
      Encyclopedia of  Chemical Technology.  3rd ed.  John Wiley
      and Sons, New York.  Vol. 23, pp. 98-130

NATIONAL CANCER INSTITUTE (NCI).  1979.  Bioassay of Titanium
      Dioxide for Possible Carcinogenicity.  NCI Carcinogenesis
      Technical Report Series No. 97.  Washington, D.C.  DHEW
      Publication No.  (NIH)  79-1347

NATIONAL INSTIUTE FOR OCCUPATIONAL SAFETY AND HEALTH (NIOSH).
      1984.   Registry  of Toxic Effects of Chemical Substances.
      Data Base.  Washington, D.C.  April 1984

WEAST, R.E., ed.  1981.   Handbook of Chemistry and Physics.
      62nd ed.  CRC Press, Cleveland, Ohio.  2*332 pages
Titaniua
Page 3
October 1985
                                                 [Clement Aj

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                                      TOLUENE
              Toluene has been shown  to be embryotoxic  in experimental
          animals, and the incidence of cleft palatt  increased  in the
          offspring of dosed sice.  Chronic inhalation exposure to high
          levels of toluene caused cerebellar degeneration and an irreversibl
          encephalopathy in aninals.   In humans, acute exposure depressed
          the central nervous system and caused narcosis.
         CAS Number;   108-88-3

         Chemical Formula:  CgH^CBj

         IUPAC Name:  Methylbenzene

         Important Synonyms and Trade Names:  Toluol, pheny line thane


         Cheraicaland Phyaieal Properties

         Molecular Height:  92.13

         Boiling Point:  110.6'C

         Melting foint:  -9S»C

         Specific Gravity:  0.8669 at 2Q»C

         Solubility in Water:  534.8 mg/liter

         Solubility in Organics:  Soluble in acetone, ligroin, and carbon
                                  disulfide; aiacible with alcohol,
                                  ether, benzene, chloroform, glacial
                                  acetic acid, and other organic solvents

         Log Octanol/Water Partition Coefficients  2.69

         Vapor Pressure:  28.7 mm Hg at 25*C

         Vapor Density:  3.14

         Plash Pointt  4.4*C
         Toluene
         Page 1
         October li8S
         Preening page blank     ^ _
"K                               "* '  '

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 Transport  and  Pate

     Volatilization  appears  to  be  the  major  route  of  removal
 of  toluene from  aquatic  environments,  and atmospheric reaetic
 of  toluene probably  subordinate  all  other fate  processes  (USI
 1979).   Photooxidation  is  the primary  atmospheric  fate procei
 for  toluene, and benzaldehyde Is reported to be the principal
 organic  product.  Subsequent precipitation or dry  deposition
 can  deposit, toluene  and  its  oiidation  products  into aquatic
 and  terrestrial  systems.   Direct photolytic  cleavage  of tolae
 is energetically improbable  in  the troposphere,  and oxidation
 and  hydrolysis are probably  not  important as aquatic  fates.

     The log oetanol/water partition coefficient of toluene
 indicates  that sorption  processes  may  be significant.  Howeve
 no specific environmental  sorption studies are  available,  and
 the  extent to  which  adsorption  by  sedimentary and  suspended
 organic  material  may interfere  with  volatilization is unknown
 Bioaccumulation  is probably  not  an important environmental
 fate process.  Although  toluene  is known to  be  degraded by
 microorganisms and can be  detoxified and excreted  by  mammals,
 the  available  data, do not  allow estimation of th«  relative
 importance of  biodegradation/biotraneforaation  processes.
 Almost all toluene discharged to the environment by industry
 is in the  fora of atmospheric emissions.


 Health Effects

     There is no  conclusive  evidence that toluene  is  carcino-
 genic or autagenic in animals or humans  (USEPA  1980).  The
 National Toxicologlcal Program  Is  currently  conducting an  in-
 halation carcinogenicity bioassay  in rats and mice.

     Oral  administration of  toluene  at doses as  low as 260 mg/
 produced a significant increase  in embryonic lethality in  mice
 (USEPA 1980).  Decreased fetal weight  was observed at doses
 as low as  434 mg/kg,  and an  increased  incidence  of cleft palat
 was  seen at doses as low as  867  mg/kg.  However, other researc
 have reported  that toluene is embryotoxic but not  teratogenic
 in laboratory animals.   There are  no accounts of a teratogenic
 effect in  humans  after exposure  to toluene.

     Acute  exposure  to toluene at  concentrations of 375-1*500 t
 produces central  nervous system  depression and  narcosis in
 humans (ACCIH 1980).  However, even  exposure to quantities
 sufficient  to produce unconsciousness  fail to produce residual
 organ damage.  The rat oral  LD5Q value and inhalation LC-0
 value are  5,000 ag/kg and  15,000 mg/m  , respectively.  Cnronic
 inhalation  exposure  to toluene  at  relatively high  concentrator
 produces cerebellar  degeneration and an irreversible  encephalo;
 in mammals.
Toluene
Page 2
October 198S

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      Toluene  in sufficient  amounts  appears  to have  the  poten-
 tial  to alter  significantly the metabolism  and  resulting  bio-
 activity  of certain  chemicals.  For  example, coadrainistration
 of  toluene along with  benzene or  styrene  has been shown to
 suppress  the  metabolism of  benzene  or  styrene in rats.


 Toxicity  to Wildlife and Domestic Animals

      Of five  freshwater species tested with toluene, the  dado-
 ceran Oaphnia  maana  was aost resistant to any acute effects
 (USEPA 1980).  The EC-- and LC.Q  values for all five species
 range from 12,700 to 313,000 Hi/liter.  No chronic  tests  are
 available for  freshwater species.   The two freshwater algal
 species tested are relatively insensitive to toluene with. EC--
 values of 245,000 Mg/liter  or greater being reported.   For
 saltwater species, EC_Q and LC5Q  values range froa 3,700  ug/liter
 for the bay shrinp to*I,050 ag/Iiter for  the Pacific oyster.
 The chronic value in an embryo-larval  test for  the sheepshead
 minnow is reported to  be between  3,200 and 7,700 ug/liter,
 and the acute-chronic  ratio is between 55 and 97.  In several
 saltwater algal species and kelp, effects occur at toluene
 concentrations from  8,000 to more than 433,000  ug/liter.


 Regulations and Standards

 Ambient Water Quality  Criteria  (DSEPA):

      Aquatic Life

      The available data are not adequate for establishing cri-
      teria.  However,  EPA did report the lowest concentrations
      of toluene known  to be toxic in aquatic organisms.

      Freshwater

          Acute toxicityt   17,500 ug/liter
          Chronic toxicity:  Mo available data

      Saltwater

          Acute toxicity:   6,300  ug/liter
          Chronic toxicity:  5,000  ug/liter

      Hunan Health .
                       x
      Criterion:  14.3  mg/liter

 HIOSH Recommended Standards:  375 ag/a? TWA
                              560 ag/a  STEL
Toluene
Page 3
October 19S5


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OSHA  Standards:  750 mg/m3 ,TWA
                 1,120 Bf/BJ Ceiling Level


REFERENCES

AMERICAN CONFERENCE OF GOVERNMENTAL INDUSTRIAL HYGIENISTS  (ACC
      1980.  Documentation of the Threshold Limit Valuta.   4th
      Cincinnati, Ohio.  488 pages

NATIONAL INSTITUTE FOR OCCUPATIONAL SAFETY AND HEALTH  (NIOSH) .
      1973.  Criteria for a Recommended Standard—Occupational
      Exposure to Toluene.  Washington, B.C.  DHEW Publication
      No. (NIOSH) HSM 73-11023

NATIONAL INSTITUTE FOR OCCUPATIONAL SAFETY AND HEALTH  (NIOSH).
      1983.  Rtgistry of Toxic Effects of Chemical Substances.
      Data. Bas*.  Washington, D.C.  October 1983

NATIONAL RESEARCH COUNCIL (NEC).  1980.  The Alkyl Benzenes.
      National Academy Press, Washington, D.C.

SAX,  N.I.  197S.  Dangerous Properties of Industrial Materials
      4th ed.  van NOBtrand Reinnold Co., New York.  1/258  page

U.S.  ENVIRONMENTAL PROTECTION AGENCY (USEPA).  1979.  Water-
      Related Environmental Fate of 129 Priority Pollutants.
     Washington, D.C.  December 1979.  tPA 440/4-79-029

U.S. ENVIRONMENTAL PROTECTION AGENCY (USEPA).  1960.  Ambient
     Water Quality Criteria for Toluene.  Office of Water  Regu-
      lations and Standards, Criteria and Standards Division,
     Washington, D.C.  October 1980.  SPA 440/5-80-07S

U.S. ENVIRONMENTAL PROTECTION AGENCY (USEPA).  1984.  Health
     Effects Assessment for Toluene.  Final Draft.  Environmen
     Criteria and Assessaent Office, Cincinnati, Ohio.   Sep-
      tember 1984.  1CAO-CIH-H033

WEAST, R.E., ed.  1981.  Handbook of Chemistry and Physics.
      62nd ed.  CRC Press, Cleveland, Ohio.  2,332 pages
Toluene
Page 4
October 1985

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                            TOXAPBENE
Summary
     Toxaphene  is a chlorinated organic pesticide and is per-
 sistent  in the  natural environment.  In aniaal bioassays, it
 Induced  liver cancer in nice and thyroid tumors in rats.  Toxa-
 phene  is fetotoxic and decreases speraatogenesis.  Chronic
 exposure to  toxaphene has been shown to damage the liver and
 kidneys  and  stimulate the central nervous systea in animals.
 In  humans, symptoms of acute intoxication include vomiting,
 convulsions, cyanosis, and coma.  Toxaphene is highly toxic
 to  aquatic organisms.
Background Information

     Toxaphene consists primarily of chlorinated caaphene and
a mixture of related compounds and isoaers,  in general, the
physical and chemical properties reported below are average
values.

CAS Number i  8001-35-2

Chemical Formula:  cioHioclg  (average formula)

Important Synonyms and Trade Names:  Camphechlor, chlorinated
                                     camphene, Attac, Phenacide,
                                     Strobane-T


Chemical and Physical Properties

Molecular Weigh ti  414

Boiling Point*  Greater than 120*C

Melting Points  £§-9S*C

Specific Gravityj  1.14 at 25'C

Solubility in Waters  0.4 to 3.0 ag/liter

Solubility in Organicss  vVery soluble in most organic solvents

Log Octanol/Water Partition Coefficient!  3.3

Vapor Pressures  0.2 to 0.4 mm Hg at 2S*C

Flash Point!  135*C  (closed cup)

Toxaphene
Page 1
October 1915
                               Si

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 Transport  and  rate

      Because toxaphene  it  a  complex mixture of polyehlorinated
 camphene derivatives, an inclusive assessment of  its environ-
 mental  transport and  fate  is difficult:.  Photolysis, oxidation,
 and hydrolysis do not appear to  be important lat* processes
 in aquatic systems.   It is persistent  in the environment, and
 transport  through soil, water, and air can occur  relatively
 easily.  Although little information is available, it appears
 that volatilization may be an important transport process,
 especially for the higher  chlorinated  bornane structures with
 very low solubility in  water.  Toxaphene is very  stable to
 biological and chemical degradation processes in  aerobic envi-
 ronmental  systems* but  it  does undergo partial reduction (loss
 of chloride content)  in anaerobic environments.   Accordingly,
 although biodegradation can  occur, it  depends on  transport
 of toxaphene to anaerobic  environments.  A dominant process
 in aquatic systems is direct aorption on sediments, or adsorption
 onto particulates, followed-  by deposition into sediment where
 biological and chemical reduction may occur.  The rate of loss
 of toxaphene from aquatic  systems is partially determined by
 particulate loading and quality  of the water body.  The physical
 and chemical properties of the individual toxaphene components
 determine  which compounds  will be sorbed and subsequently reduced,
 Bioaccumulation is an important  environmental process for toxa-
 phene.  Adsorption by biota  is rapid,  and significant uptake
 can occur  in natural systems.


 Health Effects

      The results of a bioassay conducted for the  Carcinogenesis
 Testing Program of the  National  Cancer Institute  Indicate that
 toxaphene  causes increased incidences of hepatocellular carci-
 nomas in mice,  and suggest that  it is carcinogenic for the
 thyroid in the rat (NCI If79).   IA1G has concluded that toxaphene
 is an animal carcinogen and  a suspected human carcinogen.
 Toxaphene  has  produced  both  positive and negative, results in
 a  series of different mutagenicity assays.  Studies concerning
 the  reproductive effects of  toxaphene  suggest that oral admin-
 istration  may  produce maternal and fetal toxicity.  However,
 toxaphene  does not appear  to have teratogenic effects.

     Acute exposure to  toxaphene causes effects due primarily
 to central nervous system  stimulation.  Subchronic exposure
 results in kidney changes, as well as changes in  blood chemistry.
 Symptoms of acute oral  toxaphene intoxication in  humans include
 vomiting,  convulsions,  cyanosis, and coma.  A minimus lethal
oral dose  of 40  mg/kg is reported for humans.  In rats, patho-
 logical effects  of toxaphene include cloudy swelling and con-
gestion of  the  kidneys, fatty degeneration and necrosis of
 the liver,  and  decreased spermatogenesis.  Toxaphene in the


Toxaphene
f age 2
October 1985
                                                                     >'

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diet  is  reported to inhibit hepatobiliary function in fats.  An
oral  LDSQ value of 40 mg/kg is reported foe the rat.  Although
there also are reports of toxaphene toxicity due to dermal
and inhalation exposure in humans and experimental animals,
most  available information concerns effects due to ingestion.


Toxieity to Wildlife and Domestic Animals

      Mean acute values for freshwater invertebrate species
range from 1.3 Mg/liter for the stonefly to 180 ug/liter for
the nidge.  Values for fish species range from 2 tig/liter for
largemouth bass to 20 Mg/liter for the guppy.  Mean species
chronic  values range from 0.03? pg/liter for the fathead minnow
to 1.8 Mg/liter for the midge.  Freshwater acute-chronic ratios
range from 71 to 265.  Species mean acute values for saltwater
invertebrates range from 0.11 ug/liter for a cope pod to 1,120 iag/
liter for the bard shell clam.  Values for fish species range
from  0.5 Mg/liter for the pinfish to 8.2 Mg/liter for the three-
spine stickleback.  A chronic value of 1.66 ug/liter is reported
for the  sheepshead minnow.  Bioconcentration factors among
aquatic  organisms range from about 1*200 to more than 50*000.
Toxaphene concentrations of from 0.15 to 1*000 ug/liter are
reported to cause deleterious effects in aquatic plant species.

      Toxaphene has a relatively high degree of toxicity in
aquatic  organisms and has resulted in fish kills and adverse
effects  on fish development and reproduction.  Although toxaphene
is relatively less toxic to birds and mammals, bioaccuaulation
may result in exposure to excessive concentrations.  Bird kills
due to toxaphene have been reported.


Regulations and Standards

Ambient Water Quality Criteria (DSEPA):

      Aquatic Lift

      freshwater

          Acute toxicity:  l.S ug/lit«7
          Chronic toxicity:  0.013

      Saltwater

          Acute toxicityi  0.070 ug/liter
          Chronic toxicity:  No available data
Toxaphene
Page 3
October If85
                           5*3

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      Hunan  Health

      Estimates of  the  carcinogenic  risks  associated with  lifetime
      exposure  to various  concentrations of  toxaphene  in water
      arei

      Risk       .                      Concentration

      10"!                             7.1 ng/liter
      10";                             0.71  ng/lit«r
      10"7                             0.07  ng/liter

 CAG  Onit Risk  (USEPA)s  1.13  (mg/kg/day)"1

 OSHA Standard;  0.5 ag/a3 TWA

 ACGIH Threshold-Liait Values:   0.5  ag/a3 TWA
                                1 ag/a4 STEL


 REFERENCES

 AMERICAN CONFERENCE OF GOVERNMENTAL INDUSTRIAL HYGIENISTS  (ACGIH) .
      1980.  Documentation of the Threshold  Limit Values.   4th ed.
      Cincinnati, Ohio.  488 pages

 EXECUTIVE OFFICE OF TBS PRESIDENT.  1971.   Ecological Effects
      of Pesticides on Ron-Target Species.   Office of Science
      and Technology, Washington, D.C.  June 1971*  220 pages

 NATIONAL CANCER INSTITUTE (NCI).  1979.  Bioassay of Toxaphene
      for Possible Carcinogenicity.  CAS No. 8001-35-2.  NCI
      Carcinogenesis Technical Report Series No. 37.  Washington,
      D.C.   DHEW publication No.  (NIH) '79-837

 NATIONAL INSTITUTE FOR OCCUPATIONAL SAFETY  AND BEALTH (NIOSH).
      1983.  Registry of Toxic Effects* of Chemical Substances.
      Data Base.  Washington, D.C.   October  1983

U.S.  ENVIRONMENTAL PROTECTION AGENCY (USEPA).  1979.  Water-
      Related Environmental Fate of  129 Priority Pollutants.
      Washington, D.C.  December 1979.  EPA  440/4-79-029

U.S.  ENVIRONMENTAL PROTECTION AGENCY (USEPA).  1985.  Health
      Assessment Document  for Olehloroaethane  (Methylene Chloride).
      Offie* of Health and Environmental Assessment.  Washington,
      D.C.  February 1985.  EPA  600/8-82/004F
                         *<
U.S.  ENVIRONMENTAL PROTECTION AGENCY (USEPA).  1980.  Ambient
      Water Quality Criteria for Toxaphene.  Office of Water
     Regulations and Standards, Criteria and Standards Division,
     Washington, D.C.  October  1980.  EPA 440/5-80-076
Toxaphene
Page 4
October 1985
                                                                    J

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 wtA5T, R.L., eo.   I9tait   aanaoooK o£  Cneaistry and  pnysics
      62nd «d.  CSC Press, Clevelana,  Ohio.   2,332 pages
Toxaphene
Pag* S
October 1905

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                                  TRICHtOROitftZENE


~~*       Suimaary    ,                                      '             •

              High doses of trichlorobenzene (TCB) have been shown to
         be embryotoiie to the offspring of exposed rats.  Pernal applic;
         tions of TCB increased the incidence of amyloidosis in • number
         of organs in nice and consequently shortened the animals' life-
         spans.  Inhalation exposure to trichlorobenzene had minor effect
         on the liver and kidneys in several species of eiperinental
         animals; in a study in Bice, it also damaged the bone narrow.


         CAS Number:  1,2,3-TCB:  87-61-6
                      1,2,4-TCB:  120-82-1
                      l,3,S-TCBs  108-70-3

         Chemical Formula:  CgE-Cl*

         IUPAC Nanes:  1,2,3-Trichlorobenzene;  1,2,4-Trichlorobenzene;
                       If3fS-Trichlorobenzene

         Important Synonyms and Trade Names:  Trichlorobenzene, TCB


         Chemical and Physical Properties

         Molecular weight!  181.45

         Boilinf Pointt  1,2,3-TCBt  21f»C
                         1,2,4-TClJ  213»C
                         1,3,5-TCBs  20I*C

         Melting Points  1,2,3-TCB;  54*G
                         1,2,4-TCBs  17«C
                         1,3,5-TCB:  64 *C

         Specific Gravityi  1,2,4-TCBt  1.4542

         Solubility in Waten  1,2,4-TCB:  30 »g/liter at 25*C

         Solubility in Organicsi  Sparingly soluble in alcohol; freely
                                  soluble in benzene and carbon disulfide

         Log Octanol/Water Partition Coefficient!  1,2,3-TCB:  4.1
                                                   1,2,4-TCB:  4.3 (calcu!

         Vapor Pressure:  Approziaately 0.4 am  Hg at 25*C
         Trichlorobenzene
         Page  1                                        ^
         October 19 8 5                                  Oo«m«rtt. AMOC*
        Preceding page blank

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 Transport and fate
            in little Information en th*  transport and fate  of
 trichlorobenzenes,  and what is  available priaarily concerns
 1,2,4-triehlorobentene (1,2,4-TCB).  Although  there la no  inform
 tion on the sorption of 1,2,4-TCB to soils  and sediments,  the
 high log octanol/water partition coefficient suggests that
 this compound would be adsorbed to organic  materials in soil
 and sediment.  The  volatility of 1,2,4-TCB  is  relatively low,
 but it has been found to volatilize readily from  aerated and
 quiescent waters, with a half-life of less  than 1 hour and
 4*7 hours in each medium, respectively.   Thus, air transport
 is also likely.  Sorption to suspended solids  does,  however,
 reduce the rate of  volatilization.

      1,2,4-TCB has  been shown to be oxidized in the  atmosphere
 via attack by hydroxyl radicals.  It is  not known if the conpour
 is broken down through photolysis or hydrolysis.   Biodegradatior
 of 1,2,4-TCB has been shown to  occur in  waste  treatment studies.
 However, in the environment biodegradation  is  expected to be
 slower .
 Health  Effects

      There  are  no  reports  indicating carcinogenic, teratogenic,
 or  nutagenic  activity of the  trichlorobenzenes  in humans  or
 animals,  no  specific reproductive effects  have been  found
 for the TCBs, but  embryotoxicity  has been noted at a  dose leve
 that produces maternal toxicity in rats  (Kitchin and  Boron
 1983) .
      Several  aniaal  studies  on  the subchronic toxicity of
chlorobenzenes  have  been  reported.  Inhalation studies with
1,2,4-TCB of  1.5 to  € months duration  in rats, rabbits, dogs,
and monkeys have not shown major  irreversible effects, although
some  effects  on liver and kidney  were  found  (transient histo-
logical changes and  increased relative liver weight i Rociba
et al. 1981,  Coate et al. 1982).  Increased urinary porphyrin
levels were also noted  (Xociba  et al.  1981).  Zub  (1978) reports
that  mice exposed to TCB  (i sowers unspecified) for 3 weeks
to 3  months showed indications  of bone marrow damage.  In a
chronic study in which mice  were  administered 1,2,4-TCB by
dermal application,  there was a treatment-related  increase
in the incidence of* amyleidosis,  which affected a  number of
organs and was  considered a  primary cause of death  (Tamamoto
et al. 1982).

      TCB is an  inducer of the microsoaal mixed function oxidases
and therefore will increase  metabolism, leading to the inacti-
vation or activation of chemicals affected by this system.
Trichlorobenzene
?»ge 2
October 1985

-------
 Toxieity  to wildlife  and Domestic Aniaals

      Only 1,2,4-TCB hat been studied for its toxic  effect on
 •quatic wildlife.  Acute LC5Q values for the freshwater species
 Daphnia aagna,  rainbow troue, and fathead ainnow sre  50.2,
 1.5,  and  i.S7 at/liter, respectively.  In the saltwater species,
 the LC?0  values are 0.45 and 21.4 mg/liter for aysid  shrimp
 and shffepshead  minnow, respectively.  Chronic toiieity in the
 early life stage of the fathead minnow occurred at  concentration
 of 1,2,4-TCB that  ranged from 0.206 to 0.705 mg/liter.  In
 freshwater and  saltwater algae, the EC5Q values for 1,2,4-TCB
 on chlorophyll  are 35.3 and 8.75, respectively; and for its
 effect on cell  numbers, the EC«n values are 36.7 and  8.93 mg/lit
 respectively.


 Regulations and Standards

 Ambient Water Quality Criteria  (OSSPA)s

      The  available data are not adequate for establishing eriter

 ACGIH Threshold Limit Value:  1,2,4-TCB:  40 mg/m3 TWA


 REFERENCES

 CARLSON,  6.?.   1977.  Chlorinated benzene induction of hepatic
      porphyria.  Szperientia 33*1627-1629

 COATE, W.B., SCBOENFX5R, W.H., IOSEY, W.M., and LEWIS, T.R-  198:
      Chronic Inhalation Exposure of Rats, Rabbits, and Monkeys
      to 1,2,4-Trichlorobenzene.  NTIS 7182-227174.  27 Pp.

 KITCHIN,  K.T.,  and EBRON, M.T.  1983.  Maternal hepatic and
      embryonic  effects of 1,2,4-trichlorobenzene in the rat.
      Environ. Res. 31:362-373

 KOCIBA, R.J., LEONG,  B.K.J., and BEFHZR, R.E., Jr.  1981.
      Subchronic toxicity study of 1,2,4-trichlorobenzene in
      the  rat, rabbit  and beagle dog.  Drug Chen. Toxicol. 4:
      229-249

 TIE MERCK INDEX.   1976.  9th ed.  Windholz, M., ed.  Merck
      and  Co., Rahway, New Jersey
                      v
SCHOEHY,  R.S., SMITH, C.C., and LOPER, J.C.  1979.  Non-iauta-
      genicity for  Salmonella of the chlorinated hydrocarbons
     Aroclor 1254, 1,2,4-trichlorobenzene, airex and fcepone.
     Mutat. Res. 68:125-132
Trlchlorobenzene
Page 3.
October 1985

-------
 O.S. ENVIRONMENTAL PROTECTION AGENCY (USEPA).   1979.  Water-
      Related Environmental fat* of 129 Priority Pollutants.
      Washington, D.C.  Deceaber 1979.   EPA 440/4-79-029

 U.S. ENVIRONMENTAL PROTECTION AGENCY (USEPA).   1180.  Support
      Document.  Health Effects Test fttilai   Chlorinated Benzenes.
      Asseasuent Division,  Office of Toxic  Substances,  washingtor
      D.C.  EPA 5SO/11-80-G14

 U.S. ENVIRONMENTAL PROTECTION AGENCY (USEPA).   1980.  Ambient
      water Quality Criteria for Chlorinated Benzenes.   Office
      of Water Regulation*  and Standards* Criteria and  Standards
      Division, Washington, D.C.  EPA 440/5-80-028

 YAMAMOTO, H,, OHNOr Y., NAXAMORI, X.,  OKU7AKA,  T., IMAI,  S., anc
      TSOBORA, Y.  1982. Chronic toxicity  and carcinogenic!ty
      test of 1,2,4-trichlorobenxene on mice by  denial  painting.
      J. Kara. Med.  Assoc.  33:132-141 (Japanese? summary in
      English)

 ZDB, N.  1978.  Reactivity of the white blood cell systen to
      toxic action benzene  and its derivatives.   Aeta Biol.
      Craeoviensia 21j163-174
Trichlorobenzene
Page 4
October 1985

-------
n
                                   2,3,6-TRICHLOROBENZOIC ACID
                     2,3t«-Trichlorobenzoie acid  (2,3,6-TBA) was slightly  irri-
                tating  when applied to  the shaved skin of ale*.


                CAS  Huaberj   50-31-7

                Chemical Formula:  C-jBUCljOj

                IUPAC Name:   2,3,6-Trichlorobenzoic acid

                Important Synonyms and  Trade Names:  Benzabar, Benzac, 2,3,6-TBA
                                                    and Trysben

                Chemicaland  Physical Proper ties

                Molecular Weight:  225.45

                Melting Point:  125 to  126*C

                Solubility in Water:  8,400 mg/liter

                Solubility in Organics:  Soluble  In acetone, benzene, chloroform
                                        ethanolf ethyl acetate, ethylene  glycol
                                        •ethane!, and xylene
                                         5
                Log  Octanol/Wattr Partition Coefficient:  3.S  (calculated)

                Vapor Pressure:  Very low


                Transport and Pate

                     2,3,6-Trichlorobenaoic acid  (2,3,6-TBA) is rather persistent
                in the  environment.  It is not very volatile.  It is fairly
                soluble in water and will leach through aoils, although it
                has  a rather  high log octanol/water partition coefficient,
                which would suggest some adsorption to soil organics.  2,3,6-TBA
                is relatively resistant to photolysis and biodegradts slowly.


                Health  Effects

                     Only liaited inforaation on  the toxiclty of 2,3,6-TBA
                was  available in the sources reviewed.  Ho inforaation was
                found on the  carcinogenicity, autagenicity, or reproductive
                toxicity of this compound.  One subchronic study reported  no
                histologlcal  changes in organs of rats exposed to doses of


                2,3,6-Trichlorobenzoic  acid
                Page  1
               October 1985

-------
 750 mg/kg of the sodium salt of  2,3,6-TBA.  However,  the oral
 LD-Q in rats was reported  to b«  650-1,000 mg/kg.   2,3,6-TBA
 was slightly irritating when applied  to the shaved skin of
 •ice.                ~                                 • .


 Toiicltv to Wildlife  and Domestic Animals

      The 48-hour LC,Q values for the  blucgill and  the largeraouth
 bass w«r* 1,750  and3I,250  ag/liter, respectively.   2,3,6-TBA
 is a herbicide used primarily to control broadleaf plants.
 Therefore,  these plants will be  susceptible to  its effects.
 No other information  on the  environmental toiicity of 2,3,6-TBA
 was available in the  sources reviewed.


 RegulationsandStandards

      Ho regulations or  standards have been established for
 2,3,6-trichlorobenzoic  acid*


 REFERENCES

 HERBICIDE HANDBOOK OF THE  WEED SCIENCE  SOCIETY OF  AMERICA.
      1979.   4th  ed.   WSSA, Herbicide  Handbook Committee, Champaign
      Illinois

 LfMAH,  W.J.,  REEHL, W.F.,  and ROSENBLATT, D.H.  1982.  Handbook
      of Chemical property  Estimation  Methods!  Environmental
      Behavior of Organic Ccnpounds.   McGraw-Hill Book Co.,
      Mew fork

 TIE MERCK INDEX.  1976.  9th ed.  Mindholi, M., ed.  Merck
      and Co., Rahway, New  Jersey

 NATIONAL INSTITUTE FOR  OCCUPATIONAL SAFETY AND HEALTH (NIOSB).
      1984.  Registry  of Toxic Effects of Chemical  Substances.
      Data Base.   Washington, D.C.  October 1984

 SAX,  H.I.   1975.  Dangerous  Properties  of Industrial Materials.
      4th ed.  Van Hostrand Reinhold Co., Hew fork.  1,258 pages

 U.S.  ENVIRONMENTAL PROTECTION AGENCY  (09EPA).  1979.  Water-
      Related  Environmental Fate  of 129  Priority Pollutants.
      Washington,  D.C.   December  1979.   EFA 440/4-79-029
                     \

WEAST, 1.2.,  ed.  1981.  Handbook of  Chemistry and Physics.
      62nd ed.  CRC Press,  Cleveland,  Ohio.  2,332  pages
2,3,6-Tricblorobenzoic acid
Page 2
October 198S

-------
                       1,1,1-TRICHI.OROETHANE
 Summary
      Prtliminary results suggest that  1,1,1-trichloroethanc
 (1,1,1-TCA)  inducts liver tumors in female mice.  It was shown
 to  be mutagenic using the Ames assay,  and it causes transforma-
 tion  in cultured rat embryo cells.  Inhalation exposure to
 high  .concentrations of  1,1,1-TCA depressed the central nervous
 system; affected cardiovascular function; and damaged the lungs,
 liver, and kidneys in animals and hunans.  Irritation of the
 skin  and mucous membranes has also been  associated with human
 exposure to  1,1,1-trichloroethane.
                                   i


 CAS Number:  71-55-6

 Chemical Formula:  CH^CClj

 TUPAC {fane:  1,1,1-Trichloroethane

 Important Synonyms and  Trade Namest  Methyl chloroform, chloro-
 thene,                                      1,1,1-TCA


 Chemical and Physical Properties

 Molecular weights  133.4

 Boiling Points  ?4.1*C

 Melting Point:  -30.4*C

 Specific Gravityj  1.34 at 20*C (liquid)

 Solubility in Water i  480-4,400 ing/liter at 20«C  (several divergent
                      values were reported in the literature)

 Solubility in Organicst  Soluble in acetone, benzene, carbon
                         tetrachlorlde, methanol, ether, alcohol,
                         and chlorinated solvents

Log Octanol/Water Partition Coefficients  2.17

Vapor Pressures  123 an Bg at 20*C

Vapor Densityt  4.€3
1,1,1-Trichloroethane

Octlbir IfiS

-------
 Transport  and Fate

      1,1,1-Trichloroethane  (1»1,1-TCA) disperses from  surface
 water  primarily by volatilization,  several studies have indic-
 ated  that  1,1,1-trichloroethane may be adsorbed onto organic
 materiala  in the sediment,  but this is probably not an important
 route  off elimination  from surface water.  1,1,1-Triehloroethane
 can be transported in the groundwater, but the speed of transport
 depends on the composition  of the soil.

   **'Photooiidation by reaction with hydroxyl radicals in the
 atmosphere is probably the  principal fate process for  this
 chemical.


 Health Effects

     1,1,1-Trichloroethane  was retested for carcinogenic!ty
 because in a previous study by NCI  (1177), early lethality
 precluded  assessment  of earcinogenicity.  Preliminary  results
 indicate that 1,1,1-TCA increased the incidence of combined
 hepatocellular carcinomas and adenomas in female mice  when
 administered by gavage (NT? 1984).  There is evidence  that
 1,1,1-trichloroethane is mutagenic  In Salmonella typhimurium
 and causes transformation in cultured rat eabryo cells (DSEPA
 1980}.  These data suggest  that the chemical aay be carcinogenic.

     Other toiic effects of 1,1,1-TCA are seen only at concen-
 trations well above those likely in an open environment.  The
 most notable toxic affects  of 1,1,1-trichloroethane in humans
 and animals are central nervous systea depression, including
 anesthesia at very high concentrations and impairment  of coordi-
 nation, equilibrium,  and judgment at lower concentrations (350
 ppa and above); cardiovascular effects, including premature
 ventricular contractions, decreased blood pressure, and aensiti-
 zation  to  epinephrine-induced arrhythmia; and adverse  effects
 on the  lungs, liver,  and kidneys.  Irritation of the skin and
 •ucous membranes resulting  froa exposure to 1,1,1-trichloro-
 ethane  has also been  reported*  The oral LD«0 value of 1,1,1-
 trichloroethane in fata is  about 11,000 •g/tg.

                                          •
 Tofieitv to wildlife  and Somestic Animals

     The acute toxicity ot  1,1,1-trichloroethane to aquatic
 species is rather low, with the LC.A concentration for the
•ost sensitive species tested being 52.8 »g/l.  Ho chronic
 toxicity studies have been  done on 1,1,1-trichloroethane, but
acute-chronic ratios  for the other chlorinated ethanes ranged
 froa 2.8 to 8*7.  1,1,1-Tricholoroethane was only flighty bio-
accumulated with a steady-state bioconcentratien factor of
nine and an eliaination half-life of two days.
1,1,1-Trichloroethane
Page 2
October 1983

-------
I ,                   He  inforaation on the toxicity of 1,1,1-trichloroethane
» l              to terrestrial wildlife or domestic aniaals was available in
                the literature reviewed.
                Regulation* and Standards
                Aabient water Quality Criteria  (0SEPA)i
                     Aquatic Life
                     The available data are not adequate for establishing crite
                     However, EPA did report, the lowest values of the two
                     trlchloroethanes (1,1,1 and 1/1/2) known to be toxic in
                     aquatic organisms.
                     freshwater
                          Acute toxicityt  18 «f/liter
                          Chronic toxicity!  8.4 ing/liter
                     Saltwater
                          Acute toxieity:  31.2 ng/liter
                          Chronic toxieitys  No available data
                     Human Health
                     Criterioni  IS.4 mg/liter
                                             31
                                             Level
NIOSH Reconnended Standard:  350 ppn (1,910 mg/n35/15 min Ceilir
                OSHA Standard:  350 ppu  (1,110 ag/a3} TWA

                1SFE1ESC1S
                1NTERHATIOHAL AGENCY FOR RESEARCH OR CANCER (IARC).  1979.
                     ZARC Monographs on the Evaluation of the Carcinogenic
                     Risks of Chemicals to Humans.  Vol. 20:  Some Halogenated
                     Hydrocarbons.  World Health Organisation, Lyon, Prance.
                     Pp. 515-531
                HATIOHAL CANCER IMSTITOTE (NCI),  1977.  lioassay Of 1,1,1-
                     Trichloroethane for Possible Carcinogenicity.  CAS No. 71-
                     55-6.  SCI Careinogenesis Technical Report Series Ho. 3.
                     Washington, D.C.  DHEW Publication No. (NIH) 77-803
                1,1,1-Trichloroethane
                Page 3
                October 1915                                   faoerrwnt AMooac*»
                                        £-3?

-------
 NATIONAL INSTITUTE FOR OCCUPATIONAL SAFETY AMD HEALTH (HIOSB).
      1976.   Criteria for a Recommended Standard—Occupational
      Exposure to 1,1,1-Trichloroethane (Methyl Chloroform).
      Washington, D.C.   DBEW Publication No. (NIOSH)  76-114

 NATIONAL INSTITUTE FOX OCCUPATIONAL SAFETY AND HEALTH (NIOSHJ.
      1983.   Registry of Toxic Effect*  of Chemical Substances.
      Data Base.   Washington/  D.C.  October 1983

 NATIONAL TOXICOLOGY PROGRAM (NT?).   1984.   Annual Plan  for
      Fiscal  Year 1904.   Research  Triangle Par It, N.C.  DHHS
      Public  Health Service. .  NTP-84-Q23

 n.S.  ENVIRONMENTAL PROTECTION AGENCY (USEPA),   1979.  Water-
      Related Environmental Fate of  129 Priority Pollutants.
      Washington* D.C.   December 1979.   EPA 440/4-79-029

 U.S.  ENVIRONMENTAL PROTECTION AGENCY (USEPA).   19SO.  Ambient
      Water Quality Criteria for Chlorinated Ethanes.  Office
      of  Water Regulations and Standards, Criteria and standards
      Division, Washington, B.C.*  October 1980.  EPA  440/5-80-029

 U.S.  ENVIRONMENTAL PROTECTION AGENCY (USEPA).   1984.  Health
      Effects Assessment for 1,1,1-Triehloroethane.  Environmental
      Criteria and Assessment  Office, Cincinnati,  Ohio.   Septembe
      1904.   ECAO-CIN-H005  (Final Draft)

 VERSCHUEREN,  R.   1977.   Handbook  of Environmental Data  on  Organic
    *  Cheaieals.   Van Nostrand Reinhold Co., New York.   £59 pages

 WEAST, I.E.,  ed.   1901.   Handbook of Chemistry and Physics.
      62nd ed.  CRC Press, Cleveland, Ohio.   2,332 pages
1,1,1-Trichloroethane
Page 4
October 19SS

-------
                                 1,1,2-TlICHtOROBTHAME
           Summary
                1,1,2-Trichloroethane  induced  liver  tumors  and  pheochrorao-
           cytomas in  mice.   It  caused liver and  kidney damage  in dogs.
           CAS  Number;   79-00-5
           Chemical  Formula*   CHjClCIClj
           IDPAC Name:   1,1,2-Trichloroethane
           Important Synonym  and  Trade Namess   vinyl  trichloride,  ethane
                                                trichloride
           Chemical  and  Physical Properties
           Molecular weights   133.41
           Boiling Point:   133.8*C
           Melting Point!   -3I.5»C
           Specific  Gravityi   1.4397 at 20*C
           Solubility in Water*  4,500 rag/liter  at  20'C
           Solubility in Organicsj  Soluble in alcohol,  ether,  and  chloroform
           Log  Octanol/Water Partition Coefficient* 2.1?
           Vapor Pressures  19 ma  Hg at 20*C
           Vapor Density:   4.S3

           Transport^ jndfjite
                Volatilisation and subsequent photooiidation  in the tropos-
           phere are probably  the  primary transport and  fate  processes  for
           1,1,2-trichloroethane.   Some sorption, bioaccumulatlon,  and
           biodegradation may  occur, but  these processes are  probably
           not  very  important  processes for trichloroethane transport
           or fate.
          1,1,2-Trichloroethane
          Page  1
          October  1985
                                                            dement Aeeocma*
T'"

-------
      1,1,2-Trichloroethane  induced  heptacellular  carcinomas
 and  pheochromocytoma  of  the adrenal gland  in  male and Cenale
 •ice but  did  not produce a  significant  increase  in tumor  inci-
 dence in  nale or female  rats (NCI  197?).   It  was  not  mutagenie
 when tested using the Ames  assay.   No information was found
 concerning the reproductive toxicity or  teratogenicity of
 1,1,2-trichloroethane.   No  chronic  studies were  found on  the
 toxicity  of 1,1,2-triehloroethane but single  doses as low as
 400  mg//kf caused liver and  kidney damage in dogs.  The oral
 LD5Q value for 1,1,2-trichloroethane in  rats  is  S3S mg/kg.
   .*

 Toal'city  to Wildlife  and Domestic Animals

      The  acute LCeg values  for  1,1,2-trichloroethane  for  fresh-
 water aquatic organisms  ranged  from 18,000 to 81,700  yg/liter.
 One  chronic test was  conducted;  this indicated that the acute-
 chronic ratio for 1,1,2-trichloroethane  was around 8.7.  Ho
 information on the toxicity of  1,1,2-trichloroethane  to saltwater
 species,  terrestrial  wildlife,  or domestic animals was available
 in the literature reviewed.


 Regulations and Standards

 Ambient Water  Quality Criteria  (USEPA):

      Aquatic  Life

      The  available data  ate not  sufficient for establishing
      criteria.   However,  EPA did report  the lowest values known
      to be toxic in aquatic organisms.

      Freshwater

        Acute  toxicityi   18,000 pg/liter
        Chronic toxieitys   9,400 ug/liter

      Saltwater

        Acute  toxicityi   No available data
        Chronic toxicityt   No available data

      Human Health

      estimates  of the  carcinogenic  risks associated with  lifetime
      exposure  to  various*, concentrations of 1,1,2-trichloroethane
      in water  arei
1,1,2-Tr i chloroethane
Page 2
October 1985
                                                                   .J

-------
      Risk                        Concentration

      10**f                         6.0 yg/liter
      10"S                         0.6 yg/liter
      10"7                         0.06 jig/liter

 CAG Unit Risk  (USEPA}j   1.7xlO~2  (ag/kg/day)*1


 REFERENCES

 INTERNATIONAL AGENCY FOR RESEARCH ON CANCER  (IARC).  1979.
      IARC Monographs on  the Evaluation of Carcinogenic Risk
      of Chemicals  to Humans.  Vol. 20;  some Halogenated Hydro-
      carbons.  World Health Organization, Lyon, France.  Pp. 533-543

 NATIONAL CANCER INSTITUTE  (NCI).  1977,  Bioassay of 1,1,2-
      Trichloroethane for Possible Carcinogenicity.  CAS No. 79-
      00-5.  NCI Careinogenesis Technical Report Series No. 74,
      Washington, D.C.  DHEW Publication Bo.  (NIH) 78-1324

 NATIONAL INSTITUTE FOR OCCUPATIONAL SAFETY AND HEALTH (NIOSH).
      1983.  Registry of  Toxic Effects of Chemical Substances.
      Data Base.  Washington, D.C.  October 1983

 U.S.  ENVIRONMENTAL PROTECTION AGENCY (USEPA).  1979.  Water-
      Related Environmental Fate of 129 Priority Pollutants.
      Washington, D.C.  December 1979.  EPA 440/4-79-029

 U.S.  ENVIRONMENTAL PROTECTION AGENCY (USEPA).  1980.  Ambient
      Water Quality Criteria for Chlorinated Ethanes.  Office of
     Water Regulations and Standards, Criteria and Standards
      Division, Washington, D.C.  October 1980.  EPA 440/5-80-029

 U.S.  ENVIRONMENTAL PROTECTION AGENCY (USEPA).  1984.,  Health
      Effects Assessment  for 1,1,2-Trichloroethane.  Environmental
      Criteria and Assessment Office, Cincinnati, Ohio.  September
      1984.  ECAO-CIN-H045  (Final Draft)

 U.S.  ENVIRONMENTAL PROTECTION AGENCY (USEPA).  1985.  Health
     Assessment Document for Dichloromethane (Methylene Chloride).
      Office of Health and Environmental Assessment.  Washington,
      D.C.  February 1985.  EPA 600/8-82/004P

VERSCHUEREN, I.  1977.  Handbook of Environmental Data on Organic
     Chemicals.  Van Noatrand Relnhold Co., New York.  656 pages

WEAST, R.E., ed.  1981.  Handbook of Chemistry and Physics.
      62nd ed.  CUC Press, Cleveland, Ohio.  2,332 pages
1,1,2-Trichloroethane
Page 3
October 198S

-------

-------
                          TRICHLOROEfHYLBIB
  Summary
       Trichloroethylene (TCE)  induced hepatocellular carcinomas
  in mice and Mia  autagenic when  tested using  several aicrobial
  assay systems.   Chronic inhalation exposure  to high concentra-
  tions caused liver,  kidney,  and neural damage  and  dermatological
  reactions In animals.
  CftS  Number:   79-01-6
  Chemical  Formula:   C-HC1,
  IUPAC  Name:   Trichloroethene
  Important P-'nonyns  and  Trade  Harness   Tr ichloroethene,  TCE,
                                       and  ethylene  trichloride

  Chemieal  and  PhysieaJL Properties
  Molecular Weight:   131.5
  Boiling Point:   87»C
  Melting Point:   -73*C
  Specific  Gravity!   1.4642  at  20-C
  Solubility in Water:  1,000 ag/liter
  Solubility in Organics:  Soluble  in alcohol,  ether,  acetone,
                          and  chloroform
  Log  Oetanol/Water Partition Coefficient!   2.29
  Vapor  Pressure!  60 SRI  Hg  at  20*C
  Vapor  Densltyt   4.53
  TransportandPate
  •^^^^|i^B^MB*NHB«MMHBB|aill^^B^V«PMM«MBBHII^      V
      Trichloroethylene  (TCE)  rapidly  volatilizes  into  the atmos-
  phere  where it  reacts with hydroxyl radicals  to produce hydro-
  chloric acid, carbon  monoxide,  carbon dioxide,  and carboxylic
  acid.  This is probably the most  important transport and fate
  process for trichloroethylene in  surface  water  and in  the upper

  Trichloroethylene
  Page 1
  October 1985
Preceding page blank

-------
 layer  of  soil.  TCE adsorbs  to organic materials and can  be
 bi ©accumulated  to  son* degree.  However,  it  is unclear whether
 trichloroethylene  bound  to organic material  can be degraded
 by microorganisms  or must be desorbed to  be  destroyed.  There
 is some evidence that higher organisms can metabolize TCE.
 Trichlocoethylene  leaches into the ground water fairly readily,
 and  it is a common contaminant of ground water around hazardous
 wast*  sites.


 Health Effects

     Trichloroethylene is carcinogenic to mice after oral admin-
 istration, producing hepatocellular carcinomas (NCI 1976, NT?
 1982)*  It was  found to  be autagenic using several microbial
 assay  systems*  Trichloroethylene does not appear to cause
 reproductive toxicity or teratogenicity.  TCE has been shown
 to cause  renal  toxicity, hepatotoxicity/ neurotoxicity, and
 dermatological  reactions in animals following chronic exposure to
 levels greater  than 2,000 ng/rn  foe 6 months.  Trichloroethylene
 baa low acute toxicity;  the acute oral LO-.  value in several
 species ranged  froa 6,000 to 7,000 mg/tcg.


 Toxicity  to Wildlife and Domestic Animals

     There was  only liaited data on the toxicity of trichloro-
 ethylene  to aquatic organisas.  The acute toxicity to freshwater
 species was similar in the three species  tasted, with LC-Q
 values of about 50 ag/liter.  No &Ce0 values were available
 for saltwater species.  However, a lose of 2 ag/liter caused
 erratic swimming and loss of equilibrium  in  the grass shrimp.
 NO chronic toxicity tests were reported.

     No information on the toxicity of trichloroethylene to
 domestic  animals or terrestrial wildlife was available in the
 literature reviewed.


 Regulations and Standards

Ambient Water Quality Criteria (USEPA):

     Aquatic Toxicity

     The available data,  are not adequate  for establishing criteria,
     However, EPA did rtport the lowest values known to be
     toxic in aquatic organiams.

     Freshwater

          Acute toxicity:  45 mg/liter
          Chronic  toxicity:  Ho available data

Trichloroethylene
Page 2
October 19SS

-------
      Saltwater

          Acute toxieitys  2 mg/littr
          Chronic  toiicity:  No available data

      Human iealth

      Estimates of  the carcinogenic risks associated witfc lifetin
      exposure to various concentrations of trichloroethylene
      in  water arei

      Riak             .           Concentration

      10"!                        27 jig/liter
      10,                        2.7 jig/liter
      1G~7                        0.27 ug/littr

CAG unit Risk (osEPA)t  l.lxlo"2 (»g/kg/
-------
 U.S.  ENVIRONMENTAL PROTECTION AGENCY  (USEPA).   1980.  Ambient
      Hater  Quality Criteria  for Triehloroetnylene.  Office
      of  Water Regulations  and Standards, Criteria and Standards
      Division, Washington, D.C.  October 1910.  IPA 400/5-80-07?

 U.S.  ENVIRONMENTAL PROTECTION AGENCY  (USEPA),   1983.  Health
      Assessment Document Cor Trichloroethylene.  Review Draft.
      Washington, D.C.  EPA 600/8-82-0068

 U.S.  ENVIRONMENTAL PROTECTION AGENCY  (USEPA).   1984.  Health
      Effects Assessment foe  Trichloroethylene.  Final Draft.
      Environmental Criteria  and Assessment Office, Cincinnati,
      Ohio.  September  1984.  ECAO-CIN-H009

 U.S.  ENVIRONMENTAL PROTECTION AGENCY  (tJSEPA).   1985.  Health
      Assessment Document for Chlorofora.  Office of Health.
      and Environmental Assessment, Washington,  D.C.  September
      1985.  EPA 600/8-84/004P

 VERSCHUEREN, X.  1977.  Handbook of Environmental Data, on Organic
      Chemicals.  Van Nostrand Reinhold Co., New York.  SS9 pages

 WATERS,  E.M., GERSTNER, H.B., and HUFF, J.E.  1977.  Trichloro-
      ethylene:  1.  An overview.  J. Toxicol. Environ. Health
      2s674-?OQ

 WE AST", R.E., ed.   1981.  Handbook of Chemistry  and Physics.
      62nd ed.  CRC Press,  Cleveland, Obio.  2,332 pages
Trichloroethylene
Page 4
October 1985

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                      TRIClfcOROFiOOROMETHAWB
 Summary
      Inhalation exposure to high concentrations of trlchlorofluoro-
methane adversely affects the heart and lungs in humans and
animals.
CAS Numberi  75-69-4
Chemical Formula:  CC13F
IUPAC Ham*!  Fluorotrichloromethane
Important Synonyms and Trade Namesj  Freon-11, fluorocarbon 11

Chemical and Physical Properties
Molecular Weight:  137.3?
Boiling Points  23.82 *C
Melting Pointi  -111 *C
Specific Gravityt  1.467 at 25 *C
Solubility in Water:  1,100 mg/liter
Solubility in Organic*t  Soluble in alcohol, ether, and other
                         organie solvents
Log Oetanol/tfater Partition Coefficientt  2.53
Vapor Pressures  6«7.4 an eg at 20 *C
Vapor Densitys  5.04
Transport and Fate
     Though no specific data art available, the high vapor
pressure, low solubility, and low boiling point of trichloro-
fluoroaethant make it likely that volatilization into,the atmos-
phere is the major transport process for removal of this compound
from aqueous systems.  Once in the troposphere, trichlorofluoro-
methane remains stable and eventually diffuses upward to the
stratosphere or Is carried back to earth by precipitation.
Trichlorofluoromethane
pag* 1           .
October 19S5

-------
 Triehlorofluoroaethane that reaches the stratosphere la broken
 dovn  by  high energy, short wavelength ultraviolet light and
 thl*  process is  thought to be its priaary environmental fate.
 Chlorine atoms released by such photodiseociation processes
 are theorized by soae researchers to serve as a catalyst in
 destruction of the stratospheric ozone layer.

      Photolysis, oxidation, and hydrolysis do not appear to
 be significant environmental fate processes for trichlorofluoro-
 methane  in aquatic systeas.  The leg octanol/water partition
 coefficient of trichlorofluoroaethane indicates that adsorption
 ontd  sediaenfcs nay occur.  However* data concerning sorption
 processes are inconclusive.


 Health Effects

      Based on liaited available information, trichlorofluoro-
 aethane  does not appear to be carcinogenic in aniaals or humans.
 Results  of a National Cancer Institute Carcinogenesis Bioassay
 using nice were  negative.  However, results for rats were con-
 sidered  inconclusive because inadequate nuabers of rats survived
 long  enough to be at risk froa late-developing tumors.  Although
 genotoxicity data are scant, trichlorofluoroaethane exhibits
 no autagenie activity in Salmonella tester strains.  There
 are no available data on the teratogenicity or reproductive
 toxicity of trichlorofluoroaethane.

      In  hunans,  trichlorofluoroaethane toxicity generally in-
 volves the intentional or unintentional acute inhalation of
 high  vapor concentrations.  There are reports of severe intox-
 ication  and death under such circumstances.  The cardiovascular
 and bronchopulmonary actions of trichlorofluoroaethane are
 its two aost important toxicological features and are thought
 to be aediated at least in part by aetabolic products that
 bind  to  lipid and protein cell constituents and affect vital
 processes such as cellular oxidation.

      The  LC50 value for a 4-hour exposure with rats is 26,200 ppa,
 During exposure, sublethal doses caused rapid respiration with
 soae aild hyperactivity, while lethal doses caused hyperactivity,
 tremors,  inactivity, irregular respiration, and death within
 four hours.  Laboratory aniaals periodically exposed at high
 concentrations for several days may exhibit biocheaical changes
 consistent with  slowing of cellular oxidation.  Furthermore,
 studies with experiaental -animals suggest that Inhalation expo-
 sure to high concentrations of trichlorofluoroaethane aay produce
 various cardiovascular and circulatory abnormalities.  Both
absorption and elimination are relatively rapid in humans and
experiaental aniaals.
Tr i chlorofluoroaethane
Page 2
October IfSS
                                                                     J

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Toxicity to Wildlife and Domestic Animals

     Data concerning the toxicity of trichlorofluoromethane
to wildlife and domestic animals are not available.


Regulations and Standards

Ambient Water Quality Criteria  (USETPA) :

     Aquatic Life

     The available data are not adequate for establishing criteria.

     Human Health

     Criterion:  32.3 ing/liter  (for protection against the
                 noncarcinogenic effects of trichlorofiuororaethane
                 in ambient water)

OS HA standard:  1,000 ppra  (5,600 mg/rn3) Ceiling Level

ACGIH Threshold Liait Value:  1,000 ppn (5,600 ng/m3) Ceiling Level


REFERENCES

AMERICAN CONFERENCE OP GOVERNMENTAL INDUSTRIAL HYGXINISTS UCGIH).
     1910.  Oocunentation of the Threshold Limit Values.  4th ed.
     Cincinnati, Ohio.  488 pages

NATIONAL CANCER INSTITOTE  (NCI).  1978.  Bioassay of Trichloro-
     fluoromethane for Feasible Carcinogenicity.   (CAS No. 75-69-4)
     NCI Carcinogenesis Technical Report Series No.  106.  DREW
     Publication Mo. (Nil) 78-1355

NATIONAL INSTITDTI FOR OCCtJPATIONAL SAFETY AND HEALTH (NIOSH) .
     1983.  Registry of Toxic Effects of Chemical Substances.
     Data Base.  Washington, D.C.  October 1983

SAX, N.I.  1975.  Dangerous Properties of Industrial Materials.
     4th ed.  van Nostrand Reinhold Co.* New York.   1,258 pages

U.S. ENVIRONMENTAL PROTECTION AGENCY  (USEPA).  1979.  Water-
     Related Environmental Pate of 129 Priority Pollutants.
     Washington, B.C.  -December 1979.  EPA 440/4-79-029

U.S. ENVIRONMENTAL PROTECTION AGENCY  (USEPA).  1980.  Ambient
     Water Quality Criteria for Haloaethanes.  Office of water
     Regulations and Standards, Criteria and Standards Division,
     Washington, D.C.  October  1980.  EPA 440/5-80-051
Trichlorofluorotnethane

        1S85

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                        2,4,5-TRICHLOROPHSNOL
  Summary
       2,4,5-Triehlorophenol (2»4»I-TCP) promotes the formation
  of skin tumors in mice.  In addition, although 2,4,5-trichloro-
  phenol ha* not b*en tested in a complete carcinogenic!ty bioassay,
  2f4,6-trichlorophenol has been found to be carcinogenic in
  nice.and rats.  Oral doses of 2,4,5-TCP caused liver and kidney
  lesfpnrs in rats and rabbits.  Technical grade 2,4,5-TCP is
  sometimes contaminated with the highly toxic polychlorinated
  dibenzo-p-dioxins, which .nay significantly increase the toxicity
  of the material.
                             i
  CIS Numberi  95-95-4
  Chemical Formula:  CgHjCl-OH
  IUPAC Name:  2,4,5-Trichlorophenol
  Important Synonyms and Trade Namesj  Dowicide 2, Dowicide B,
                                       Preventol I

  Chemical and Physical Properties
  Molecular Weight:  197.5
  Boiling Point:  253*C (sublimes)
  Melting Point;  68-70.S»C
  Specific Gravityt  1.178 «t 2S»C
  Solubility in Water:  1,2000 mg/liter at 25*C
  Solubility in Organicst  Soluble in alcohol, organic solvents,
                           and llgroin
  Log Octanol/Water Partition Coefficient:  3.7
  vapor Pressure!  1 an Hg at ?2.00C
        7*0
  2,4,5-Trichlorophenol
  fig» 1
  October 1985                                     Ocianwnt Ammo&mta*
Preceding page blank

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 Transport  and  Fate

      There is  very  little  information  available on  the environ-
 mental  transport  and  fate  of  2,4,5-trichloroph«nol; however,
 there is some  information  concerning 2,4,6-trichlorophenol
 which nay  act  in  a  similar fashion.  2,4,6-Tricblorophenol
 has  a low  vapor pressure  (1 ma n§ at 76.5"C), Ilka  2,4,5-tri-
 chlorophenol,  and is  unlikely to volatilize from water.  Photo-
 oxidation  of 2,4,6-trichlorophenol occurs  in the presence of
 an electron acceptor*  and  2,6-diehlorobenzoquinone  and 2,6-
 dichlprohydroquinone  are formed.  Microbial degradation of
 2,4-;'6-trichlorophenol  has  been reported.   In a number of soil
 samples, complete degradation of the compound occurred in 1
 to 9 days  and  microbial action in acclimated sludge completely
 degraded the compound  in 5 days.  However, there is a report
 indicating that 2,4,5-trichlorophenol  is  resistent  to degradation
 by certain soil microbes,  possibly because of the meta-substi-
 tuted chlorine atom in this molecule.   Thus, the fate of 2,4,5-
 trichlorophenol in  soil say differ from that of 2,4,6-triehloro-
 phenol.


 Health Effects

      Although  2,4,S-triehlorophenol has not been tested for
 carcinogenic!ty,  the NCI bioassay on 2,4,6-trichlorophenol
 was  positive in both rats  and mice.  2,4,5-Trichlorophenol
 gave negative  results  in the  Ames mutagenicity assay, but has
 been found to  promote  the  formation of papillomas on the skin
 of mice pretreated  with the initiator  diaethylbenzanthracene.

      McCollister  et al. (1961) conducted  a number of acute
 and  subchronic studies of  2,4,5-trichlorophenol toxieity in
 rats  and rabbits,   me acute  oral LD.fl value of 2,4,5-trichloro-
 phenol was approximately 3,000 mg/kg in the rat.  Rats treated
 IS times over  24  days  with doses ranging  from 30 to 1,000 mg/kg
 did  not show adverse effects.  Bats supplied diets that gave
 daily doses of 300  and 1,000  mg of 2,4,5-trichlorophenol per
 kilogram body  weight for 98 days did show liver and kidney
 effects which  were  dose related.  Bats given lower doses did
 not  show any compound  related effects*  Rabbits given oral
 doses of 10 to 500  mg/kg for  28 days exhibited slight renal
 lesions and, at 500 mg/kg,  liver lesions.

      In vitro  studies  en the  effect of 2,4,5-trichlorophenol
on aitochondrial  oxidative phosphorylation showed that it caused
 complete uncoupling.   The  concentration of 2,4,5-trichlrophenol
 that produced  a 501 inhibition of ATP  production in isolated
mitochondria was  8  times less than the concentration of 2,4,6-
 t r ichlorophenol.
2,4,5-Trichlorophenol
Page 2
October 1985

-------
                 When considering the health effects of 2,4,5-trichloro-
            phenol, it aust be remembered that the technical  grade compound
            is contaminated with polychlorinated dibenzo-p-dioxins, including
            2,3,7,8-tetrachloEodibenzo-p-dioxin which is highly toxic and
            produces a large number of health effects in experimental animals.

                                                                        /
            Toxicity to Wildlife and Domestic Animals

                 2,4,5-Trichlorophenol was found to be acutely toxic to the
            saltwater aquatic species mysid shrimp and aheepshead  minnow  after
            a 96-hour exposure to concentrations of 3,330 and 1,660 pg/liter,
            respectively.  No chronic toxicity information on aquatic organ*
            isms was available for 2,4,5-trichlorophenol.


            Regulations and Standards

            Ambient Water Quality Criteria (DSEPA):

                 Aquatic Life

                 The available data are not adequate for establishing criteria,

                 Human Health

                 Health criterion:  2.6 mg/liter
                 Organoleptic criterion:   1.0 Mg/liter


            REFERENCES

            INTERNATIONAL AGENCY FOR RESEARCH ON CANCER (IARC).  1979.
                 larc Monographs on the Evaluation of Carcinogenic Risk
                 of Chemicals to Humans.   Vol. 20:   Some Halogenated Hydro-
                 carbons.  World Health Organization, Lyon, Prance

            NATIONAL INSTITUTE FOR OCCUPATIONAL SAFETY AND HEALTH  (NIOSH).
                 1983.  Registry of Toxic Effects of Chemical Substances.
                 Data Base.  Washington,  D.C.  October 1983

            U.S. ENVIRONMENTAL PROTECTION AGENCY (USEPA).  1979.   Water-
                 Related Environmental Fate of 129 Priority Pollutants.
                 Vol.  2,  Washington, D.C.  December 1979. EPA  440/4-79-029

            U.S. ENVIRONMENTAL PROTECTION AGENCY (USEPA).  1980.   Ambient
                 Water Quality Criteria for Chlorinated Phenols.   Office
                 of Water Regulations and Standards, Criteria and  Standards
                 Division, Washington, D.C.  October 1980. EPA  440/5-80-032
            2,4,5-Tri chlor ophenol
            Page  3
            October  1985
TLA                               SS\

-------
 D.S.  EKV1RONMENTAL PROTECTION AGENCY  (USEPA).   1904.  Htalth
      Effects Assessment  foe  2,4>5-Trichlorophenol.  Environmental
      Criteria  and A»»tssn«nt Offie*f Cincinnati, Ohio.  September
      1984.  ECAO-CIN-H034   (flnftl Draft)

      t  R*E*t *d.  1981.  Handbook of Chemistry  and Physics.
      62nd *d.  C1C Press, Cleveland, Ohio.   2,332 pages
2,4,5-Trichlorophenol
fag* 4
October 1985
                                                                  J

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                2,4,5-TRICHLOROPIENOXYACETIC ACID
     2,4,5-Trichlorophenoxyacetic »cid  (2,4,5-T) is one of
the major constituents of Agent Orange, the major defoliant
used in Vietnam,  it is commonly contaminated with TCDD, an
extremely toxic material that may be responsible for soae of
the effects associated with exposure to technical 2,4,5-T.
These effects include chloracne and the induction of microsomal
nixed function oxidase activity.  Administration of purified
2,4,5-T has been shown to cause fetal loss, disrupt fetal develop-
ment, and induce fetal malformations.


CAS Number:  93-76-5

Chemical Formula:  CljCgHjOCHjCOOB

IUPAC Name:  2,4,5-Trichlorophenoxyacetic acid

Important Synonyms and Trade Names:  Brushtox, Ded-weed Brush*
                                     Killerf 2,4,5-T, Heedar


Chemical and Physical Properties

Molecular Weighti  255.48

Melting Point*  153«C

Solubility in Water:  250 rag/liter

Solubility in Organics:  Soluble in alcohol

Vapor Pressures  Less than 8.4 x 10   mm Eg at 2S*C

Vapor Density:  8.S3

pKa:  2.84


Transport and Fate

     Photodecomposition of 2,4,5-trichlorophenoxyacetic acid
(2,4,5-T) in water can occur by a number of different mechanisms.
These include photooxidation of the phenoxy side chain and
photonucleophilic displacement of Cl by OH to fora chlorophenols,
and photoreductive dechlorination to fora phenoxyacetic acids.
Photolysis of 2,4,5-T under dry conditions is also a significant
2,4,5-Tri chlorophenoxyacetic acid
Page 1
October 1985
                                                              ate*

-------
 environmental fit*.   Because of  its  low vapor  pressure,  vola-
 tilisation of this conpound  is not likely to be  an important
 process.   At least one  experimental  study confirmed that vola-
 tilization of 2,4,S-T fcon an aqueous  solution is  negligible.

      2,4,5-T is only weakly  adsorbed to soil.  In  addition,
 this conpound is moderately  soluble  in water,  and  experimental
 studies snow that sone  leaching  of 2,4,S-T Icon  soil does occur.
 This material has been  found at  low  concentrations in groundwater
 underlying areas to  which it has been  applied*   It has also
 been detected in the initial rainwater runoff  in treated areas.
 However, nost 2,4,5-T xenains in the upper layers  of soil,
 and  leaching is not  thought  to be a  major transport process.

       The  environmental persistence  of 2,4,5-T is  relatively
 low.   For  example, 2,4,5-T residues  in a forest  reportedly
 declined by 50% in € weeks and by 901  in 6 months.   Bioaecumu-
 lation of  2,4,5-T does  not appear to be  a significant environ-
 mental process.


 Health Effects

      Currently, there is no  conclusive evidence  that 2,4,5-T
 is carcinogenic in humans or experimental aniaals.   Data from
 studies on experimental animals  and  in vitro studies suggest
 that  2,4,5-T is not  mutagenic but may  damage chromosomes.  Ad-
 ministration of 2,4,5-T to pregnant  experimental animals dis-
 rupts fetal  development, causing fetal loss, developmental
 retardation,  and malformations or anomalies.   Other acute or
 chronic effects of 2,4,S-T have  not  been adequately demonstrated.
 An oral LD5Q  level of 300 ag/kg  is reported foe  the rat.

      The toxic  effects  of purified 2,4,5-T..in  experimental
 animals and  humans have not  been adequately studied, and  other
 toxic effects observed  as a  result of  exposure to  2,4,5-T..for-
 mulations,  including induction of aicrosoaal mixed  function
 oxidase activity and chloracne,  may  actually be  caused by
 2,3,7,8-tetrachlorodibenzo-p-dioxin  (TCDD), a  common contaminant
 of these- formulations.  Information  concerning these and  other
 toxic effects Is presented in the chemical profile  on TCDD.


 Toxicity to Wildlife and Domestic Animals

      Limited  evidence suggests that  2,4,5-T may  affect wildlife
 or domestic  aniaals  indirectly by disrupting vegetation  density
 and composition in an area.   Herbivores  may be affected  by
 changes in the  types and amounts  of  their potential food  sources.
These  changes may favor sone species and be detriaental  to
 others.  Other  animals  may lose  sources  of cover from predators
 or sites for  nest and den building.


 2,4,5-Trichlorophenoxyacetic acid
Page  2
October 1985

-------
     Virtually no specific Information on the toxicity of 2,4,5-T
to wildlife or domestic animals is available.  While 2,4,5-T
Is thought to have relatively low toxicity for vertebrate species,
it ha* been reported that populations of invertebrates, including
beneficial insect species, have been adversely affected at
field concentrations.  Invertebrates nay be adversely affected
both directly because of the compound*s tosieity and indirectly
because of the changes 2,4,5-T produces in vegetation growth
patterns.  Although 2,4,5-T is not reported to have large,
direct toxic effects on livestock, there are reports of animal
deaths due to alterations in plant chemistry and palatability
after 2,4,5-T treatment.

     Information on the effects of 2,4,5-T on aquatic species
is also limited.  Among fish, the LD.* value for perch is
55 mg/liter> for guppies, S mg/liter? and for rainbow trout,
1.3 mg/liter.


Regulations and Standards

OSHA Standard (air):  10 ag/m3 TWA

ACGIH Threshold Limit Value:  10 ag/m3 TWA


REFERENCES

AMERICAN CONFERENCE OF GOVERNMENTAL INDUSTRIAL HYGIENISTS (ACGIH).
    . 1980.  Documentation of the Threshold Limit Values.  4th
     ed.  Cincinnati, Ohio.  488 pages

INTERNATIONAL AGENCY FOR RESEARCH OH CANCER (IARC).  1977.
     IARC Monographs on the Evaluation of the Carcinogenic
     Risk of Chemicals to Man.  Vol. 15:  Some Fuaigants, the
     Herbicides, 2,4-D and 2,4,5-T, Chlorinated Dibenzodioxins
     and Miscellaneous Industrial Chemicals.  World Health
     Organization, Lyon, France.  Pp. 273-299

THE MERCK INDEX.  1976.  9th ed.  Windholz, M., ed.  Merck
     and Co., Rahway, Hew Jersey

NATIONAL INSTITUTE FOR OCCUPATIONAL SAFETY AND HEALTH (NIOSH).
     1984.  Registry of Toxic Effects of Chemical Substances.
     Data Base.  Washington, D.C.  October 1984

NATIONAL RESEARCH COUNCIL OF CANADA.  1978.  Phenoxy Herbicides;
     Their Effects on Environmental Quality.  Subcommittee
     on Pesticides and Related Compounds, Ottawa, Canada.
     NRCC No. 16075.  440 pages
2,4,5-Trichlorophenoxyacttic acid
Page 3
October 1985
                                                         Aeaa

-------
 SAX, H.I.  1975,  Dangerous Properties of Industrial Materials.
     4th ed.  Van lioatrand Reinhold Co., New York.  1,258 pages

 V2RSCHUERZN, K.  19??.  Handbook of Environmental Data on Organic
     Chemicals.  Van Hottrand Reinhold Co., Rew York.  659 pages

 VETERANS ADMINISTRATION (VA).  1982.  Review of Literature
     on Herbicides, Including Phenory Herbicides and Associated
     Oioiina.  Volt. 1 and 2i  Analyiis of Literature and Bibli-
     ography.  Department of Medicine and Surgery, Washington, D.<

 VETERANS ADMINISTRATION (VA).  1984.  Review of Literature
     on Herbicides, including Phenoxy Herbicides and Associated
     Dioxins.  Vols. 3 and 4.  Analysis and Bibliography of Re-
     cent Literature on Health Effects.  Department of Medicine
     and Surgery, Washington, D.C.
2,4,5-Trichlorophenoxyacetic acid
Page 4
October 1985

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             2-(2,4,5-TRXCHLOROPHEHOXY)PROP20NIC ACID
Summary
     2-(2,4,5-Trichlorophenoxy)propionie acid  (2,4,5-TP, Sllvex)
is a broad spectrum herbicide that is commonly contaminated
with TCDO.  The toxic effects associated with exposure to 2,4,5-
TP are generally considered to be caused by this contaminant.
Howeverr pure 2,4,5-TD may have an adverse effect on reproduction
that is not attributable to TCDD.


CAS Numbers  93-72-1

Chemical Formula:  CLjCgHjOOMCHjJCOOH

IUPAC Name:  2(2»4,S-frichlorophenoxyjpropionic acid

Important Synonyms and Trade Names:  Sllvex, 2,4,5-TCPPA, Fenoprop,
                                     luran, 2,4»5-TP


Ch emiea1 and Physieal Properties

Molecular Weight:  219.53

Melting Point:  111.S*C

Specific Gravity:  1.640 at 30*C

Solubility in Wattt:  ISO mg/liter

Solubility in Organics:  Soluble in acetone, benzene, carbon tetra-
                         chloride, ether, heptane, and aethanol

Log Octanol/Water Partition Coefficient:  4 (calculated)

Vapor Pressure:  Less than 1 ma Eg at 20*C


Transportand Pate

     2(2,4,S-Trichlorophenoxy)propionic acid (2,4,5-TP) is not
very soluble in water and has a low vapor pressure.  It prob-
ably is not readily transported in the environment and is likely
to be fairly persistent.^  However, it may volatilize to some
degree because of its high activity coefficient in water.
Adsorption to soil and sediments is probably an important fate
for 2,4,5-TP.  Photooxidation and blodegradation Bay be the
ultimate fate processes in the environment, but neither is
expected to occur very quickly (Bailey et al.  1970).


2,4,5-TP
Page 1
October 1985

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Health Effects

      2,4,5-TP is contaminated with aaall amounts of  2,3,7,8-
tetrachlorodibenzo-p-dioxin  (TCDD), and the toxic effects of
2,4,5-TP ic* generally  believed Co bt caused by this contaain-
•tion.  Thtrt Is suggestive evidence/ however, that 2,4,5-TP
may  have adverse effects on reproduction that are not attrib-
utable to TCDD.  This conclusion is based on a comparison of
studies using 2,4,5-TP  and other atudies using essentially
uncontaoinated 2,4,5-trichlorophenoxyacatic acid (2,4,5-T).
Oncontaainated 2,4,5-T  and uncontaainated 2,4,5-TP are closely
related compounds and are considered to have siailar effects
(Gehring 1980).
      The toxic effects  of 2,4,5-TP have not been studied veil,
but  they are probably siailar to those caused by 2,4,5-T and
low  levels of TCDD.
Toxicity to Wildlife and Domestic Aniaala

     The 96-hour LC-Q values for 2,4f5-TP in rainbow trout
and bluegills were 15 and 10 mg/liter, respectively.  In 5-day
feeding studies, Japanese quail had an LD50 value greater than
5,000 ppta of 2,4,5-TP when administered in the diet.  Ring-
necked pheasants under the sane regime had an LC«* of about
4,500 ppn.  2,4,5-TP is a broadleaf herbicide.


Regulations and Standards

     IPA has banned the use of 2,4,5-T? on turf and in aquatic
systems.


REFERENCES

AMERICAN CONFERENCE OF GOVERNMENTAL INDUSTRIAL KQXEHX5TS. (ACGIH)
     1180.  Docuaentation of the Threshold Liait Values.  4th
     ed.  Cincinnati! Ohio.  4IS pages

BAILEY, G.W., THURSTON, A.D., POPE, J.D., JR., and COCBRANE, D.R.
     1970.  The degradation kinetics of an ester of silvex
     and the persistence of silvex In water.  Weed Science
     18i413-418
                       *.
GEHRING, P.J.  1980.  Direct Testimony of Or. Perry J. Gehring.
     In Rei  The Dow Chemical Company et al. (2,4,5-T and Silvex
     cancellation hearing).  Exhibit 912.  Firm Docket Mo." 415
     et al. U.S. environmental Protection Agency
2,4,5-TP
Page 2
October 1985
                                                                  J

-------
 HERBICIDE  HANDBOOK OP THE WEED SCIENCE SOCIETY OF AMERICA.
      4th ed.  NSSA Herbicide Handbook Committee, Champaign,
      Illinois

 LYMAN, W.J., REEHL, W.F., and ROSENBLATT, D.H.  1982.  Handbook
      of Chemical Property Estimation Methods:  Environmental
      Behavior of Organic Compounds.  McGraw-Hill Book Co.,
      New fork

 THE MERCK  INDEX.  1976.  9th *d.  Windholz, M.f td.  Merck
      and Co., Rahway, New Jersey

 NATIONAL ACADEMY OP SCIENCES (HAS).  1977.  Drinking Mater
      and Health.  Safe Drinking Hater Committee, Washington, D.C.
      939 pages

 NATIONAL INSTITUTE FOR OCCUPATIONAL SAFETY AND HEALTH (NIOSH),
      1984.  Registry of Toiie Effects of Chemical Substances.
      Data  Base.  Washington, D.C.  October 1984

 VETERANS ADMINISTRATION (VA).  1981.  Review of Literature
      on Herbicides, Including Phenoxy Herbicides and Associated
      Dioiins.  Vols. I-IV.  Department of Medicine and Surgery,
      Washington, D.C.

 WEAST, R.E., ed.  1981.  Handbook of Chemistry and Physics.
      62nd  ed.  CRC Press, Cleveland, Ohio.  2,332 pages
2,4,5-TP
Page 3
October 198S
                        SSI

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                   TRIS(2,3-DIBROMOPROPYL)PHOSPHATE
   Summary
        trit(2,3-Dibronopropyl)phosphate  (TRIS)  Is probably per-
   •istent  in  the environment.  It  is carcinogenic;  it  induces
   tumors of the forestomach, lung, kidney, and  liver in alee
   and  rats after oral administration and tumori of  the forestomaeh,
   lung, skin, and mouth  in nice after dermal application.  TRZS
   is also  mutagenic.  Dermal application caused testicular atrophy
   and  kidney  damage in rabbits.  In humans, dermal  exposure may
   produce  allergic skin  reactions  in susceptible individuals.


   CAS  Number:  12S-72-7

   Chemical Formulas   (CHjBrCHBrCHjO)3PO

   Important Synonyms and Trade Names:  2,3-Dibromc-l-propanol phos-
                                       phate; tris(2,3-ibromopropyl)
                                       phosphoric acid ester; TRIS


   Chemical and Physical Properties

   Molecular Weight:  697.7

   Melting  Point:  5.5«C

   Specific Gravity:  2.27 at 25»C

   Solubility  in Water:   Insoluble

   Solubility  in Organicsi  Soluble in all proportions  in carbon
                           tetrachloride, chloroform, methylene
                           chloride

   Vapor Pressure:  0.00019 mm Hg at 25*C


   Transport and fate

       The limited information available concerning tris(2,3-dibro-
   mopropyl)phosphate  (THIS} suggests that this compound is relative-
   ly persistent in the environment.  Hydrolysis, oxidation, and
   photodegradation are not likely to be significant fate processes.
   Although slow biodegradation of TRIS in raw sewage is reported
   to occur, it is not thought to b« an important environmental
   process.
  TRIS
  Page 1
  October 1985
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     Given  its  low  vapor pressure,  volatilisation of THIS  and
 subsequent  atmospheric  transport  is not likely  to be a  signifi-
 cant process.   Because  this  compound  is virtually insoluble
 in water, adsorption  to particulate natter and  sediaent may
 be an  important environmental  transport process.  80 adequate
 empirical data  concerning  the  potential for bioconcentration
 and bioemgnification  of THIS are  available.  However, because
 this compound has low solubility  in water and is readily soluble
 in organic  solvents,  these environmental processes are  likely
 to occur to soae extent.


 Health Effects

     There  is sufficient evidence that THIS is  carcinogenic
 in nice and  rats, and can  produce tumors of the forestomach,
 lung, kidney, or liver  after oral administration  (NCI 1978).
 This compound also  produces  benign  and malignant tumors of
 the forestomach, lung,  skin, and  oral cavity after dermal  applica-
 tion in mice (Van Duuren et  al. 1978, in IARC 1979).  TRIS
 is also mutagenic in  a  number  of  test systems.  Based on a~
 limited number  of experiments, there  is no evidence that THIS
 is teratogenic  in laboratory animals.  THIS is  reported to
 cause testieular atrophy and kidney damage in rabbits after
 application  to  the  skin for  3  months.  This compound has an
 oral LD.g of 5.24 g/kg  in  rats.   THIS, does not  appear to present
 a significant acute toxic  hazard  in humans.  However, ingestion
 of this compound is reported to cause some abdominal discomfort
 and gastrointestinal  irritation.  Dermal exposure may produce
 allergic contact sensitization in some subjects.


 Toxieity to  Wildlife  and Domestic JUiimals

     practically no information concerning the  toxicity of
 THIS to wildlife and domestic  animals exists.   Exposure to
 concentrations  of 1 mg/liter caused 501 mortality to goldfish
 within 4 days (Gutenmann and Lisk 1975) in one  study.  Central
 nervous system  effects  were  seen  in the fish prior to death.
 Using a model based on  the solubility of selected chemicals
 in water, a  biomagnification potential (concentration in fish/con*
 centration  in water) of 338  has been  calculated for TRIS.


 Regulations  and  Standards

     The manufacture and use of the flame retardant tris(2,3-
 dibromopropyl)phosphate has  been  banned in the  United states.
TRIS
Page 2
October 1985

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 REFERENCES

 GUTENMANN, W.H. and LISK, D.J.   1975.  flame retardant  release
      from fabrics during laundering and their toxicity  to fish.
      Bull* Environ. Contain. Toxicol. 14:61-64

 INTERNATIONAL AGENCY FOR RESEARCH ON CANCER  (IARC).  1979.
      1ARC Monograph! on the Evaluation of Carcinogenic Risk
      of Chemicals to Humans.  Vol. 20:  Some Halogenated Hydro-
      carbons.  World Health Organization/ Lyon, France.
      Pp. 57S-588

 NATIONAL CANCER INSTITUTE (NCI).  Bioassay of Tria  (2,3-Dibromo-
      propyl) Phosphate for Possible Careinogenicity.  (CAS
      So.126-72-7) NCI Carcinogenesis Technical Report Series
      No. 76.  Washington, D.C.   DHEW Publication No. (NIB)
      78-1326

 NATIONAL INSTITUTE FOR OCCUPATIONAL SAFETY AND HEALTH (NIOSH).
      1984.  Registry of Toxic Effects of Chemical Substances.
      Data Base.  Washington, D.C.  October 1984

 D.S..  ENVIRONMENTAL PROTECTION AGENCY (OSEPA) .  1976.  A Study
      of Plase Retardants for Textiles.  Washington, D.C*
      February 1976.  EPA 560/1-76-004

 D.S.  ENVIRONMENTAL PROTECTION AGENCY (USEPA).  1976.  Investi-
      gation of Selected Potential Environmental Contaminants:
      Baloalkyl phosphates.  Washington, D.C.  August 1976.
      EPA 560/2-76-007
TRIS
Page 3
October 1985

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                             VANADIUM


Summary

     Occupational exposure to airborne vanadium has b«en shown
to irritatt the akin, eyes, and respiratory tract and to cause
bronchitis, bronchospssms, and chest pain.  Oral exposure has
been associated with gastrointestinal disturbances and discolor-
ation of the oral mucosa.  Chronic exposure to vanadium nay
have an adverse effect on various enzyme systems.


Bacfcground Informat1on

     Vanadium can exist in the 0, +2, +3, +4, and +5 oxidation
states.  Elemental vanadium is insoluble in water.  Vanadium
usually occurs in some oxidized form, and soluble and insoluble
vanadium compounds can occur.  Vanadium can bind covalently
to organic molecules to yield organometallic compounds.

CAS Numbert  7440-62-2

Chemical Formulas  V

IOPAC Name:  Vanadium


Chemical and Physical Properties

Atomic Weight:  50.9

Boiling Point»  3,380*C

Melting Point;  1,890*C

Specific Gravitys  5.96

Solubility in Water:  Insoluble


Transport and Fate

     The extent to which vanadium is transported in aqueous
media is largely determined by the chemical species present
and by environmental factors determining its solubility and
binding bo organic materials.  Some vanadium compounds are
volatile, and atmospheric transport of fumes as well as partic-
ulates can occur.  Some bioaccunulation of vanadium occurs.
However, in mammals, it appears that excess vanadium can be
rapidly excreted in the urine.  In humans, it Is excreted as
sodium metavanadate or ammonium vanadyl tartiate.
Vanadium
fage 1
October 1985
 Preceding page blank

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 Health  Effects

      There  art  no  data  available  bo suggest that vanadium  has
 carcinogenic, mutagenic,  teratogenic, or  reproductive  effects
 in  humans or experimental animals.  Occupational exposure  to
 airborne vanadium  compounds can produce eye and *kln irritation.
 Oral  exposure may  produce gastrointestinal disturbances and
 diaeoloration of the oral mucosa  and tongue.  There la no  evidence
 of  chronic  oral toxtcity. The most important toxic effects
 of  vanadium are associated with inhalation exposure.   Symptoms
 include acute upper and lower respiratory Irritation with  aucous
 discharge and bronchitis/ cough,  bronchospasm, and chest pain.
 Acute effects are  reported to occur at concentrationos as  low
 as  0.1  rag/m .   Effects  on various enzyme  systems may also  occur,
 especially  after chronic  exposure.

      Vanadium is toxic  to experimental animals by all  routes
 of  administration.  Its toxicity  generally increases with  valence
 number.  The pentavalent  chemical forms,  such as vanadium  pent-
 oxide and the vanadates are the most toxic compounds.  In  albino
 nice, an oral LD-Q of 130 mg/kg vanadium  trioxide Is reported;
 a value of  23 rag/Kg is  reported for vanadium pentoxide and
 vanadium trichloride.


 Toxieity to Wildlife and  Domestic Animals

      Only limited  Information was available on the toxicity
 of  vanadium to  aquatic  organisms  {2A 1985}.  Freshwater fish
 had 96-hour LC.Q values ranging from 5,000 to 100,000  pg/liter
 and generally around 10,000 jig/liter.  Daphnids were the only
 Invertebrates studied;  a  96-hour  LC§0 value of les than 0.16 ug/lit
 was reported.   Chronic  toxicity (5 to 28  day LC.n values)  was
 generally seen  at around  2,000 |jg/liter;  the lowest value
 reported was 500 ug/liter for a 6-day LC5Q value in the guppy.

      Adequate data are  not available for  characterization  of
 toxicity to wildlife and  domestic animals.  Calcium vanadate
 was fatal to a  group of chicks fed a diet containing 200 to
 600 ppm for 11  to 32 days.


 Regulations and Standards

 NIOSH Recommended standards!  I «g/m3 TWA
                             O.OS mg/m3 Celling Level

AC6Z1 Threshold Limit Valuei

     O.OS mg/m3 (vanadium pentoxide* respirable dust and fume)
Vanadium
Page 2
October 1915

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 REFERENCES

 AMERICA CONFERENCE OF GOVERNMENTAL INDUSTRIAL HYGI1NISTS  (ACGIHJ
     1980.  Documentation of the Threshold Liait Values.   4th ed.
     Cincinnatir Ohio.  4SS pages

 DOOLL, 3., RLAASSEN, C.D., and AM5UR, M.O., eds.   If80.  Casarett
     and Doull's Toxicology:  Tht Basic Science of Poiions.
     2nd ed.  Macrelllan publishing Co., Rev York.  778 pages

 EA ENGINEERING, SCIENCE, AND TECHNOLOGY, INC.  (EA).  1985.
     Vanadium:  Environmental and Community Health Impact.
     Prepared for American Petroleum Institute, Washington
     D.C., January 1185.  EA Report API 37 0

 NATIONAL ACADEMY OP SCIENCE (NAS).  1977.  Drinking Water  and
     Health.  Safe Drinking Water committee, Washington, D.C.
     939 pages

 NATIONAL INSTITUTE POR OCCUPATIONAL SAFETY AND HEALTH  (NIOSI).
     1977.  Criteria for a Recommended Standard—Occupational
     Exposure to vanadium.  Washington, D.C.  DHEW Publication
     No. (NIOSI) 77-222

 NATIONAL INSTITUTE FOR OCCUPATIONAL SAFETY AND HEALTH  {NIOSH5.
     1984.  Registry of Toxic Effects of Chemical Substances.
     Data Base.  Washington, D.C.  July 1984

 WIAST, ft.!., ed.  1981.  Handbook of Chemistry and Physics.
     62nd ed.  CRC Press, Cleveland, Ohio.  2,332 pages
Vanadium
Page 3
October 1985

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                           VIHYL CHLORIDE
 Summary
      Vinyl chloride la a huaan carcinogen that cauaaa angioaar-
 eoaas of the liver and tuaora of the brain, lung/ and haaolyapho-
 polette ayatea.  Thara la auggeatlvt avldenca that vinyl chloride
 haa teratogenic and reprodaetlva affteta In both huaan* and
 anlajala.  Chronic huaan axpoaura to vinyl chloride la aasoclated
 with" nultipl* a.y*t«ale dlaocdacar Including a aeltEOtle »yndrone,
 aero-oat•olysifr and liv«r daa«f«.  Aeut* huaan axpoaura to
 high conctntrations can eauaa narcoais, raaplratory tract irrita-
 tion, bronchitia, and aaaory dlatuzbancaa.  Chronic «ipoauf»
 by anlaala can raault In laalona of th* llvarf kldnaya, spleen,
 and lunga.
 CAS Ku*b*rs  71*01-4
 Chemical Foraulat  CHjCHCl
 IUPAC Naaai  Chloro*th«na
 Important Synonya* and Trade Naaaai  Chloroathylana, VC, aono-
                                      chloroathylana
 Chanlcal and Phyiical Propertiea
 Molecular Weighti  62.5
 Boiling pointi  -1J.37*C
 Malting Point»  -153.8«C
 Specific Gravityt  0.9106 at 20*C
 Solubility In Watari  1,100 «g/liter at 2S*C
 Solubility la Of guiles i  Soluble) la alcohol athar and carbon
                          tetrachlpride
 Log Octanol/Water Partitibn Coefficient!  1.4  (eatiaated)
 Vapor Preaaurai  2,iiO mm Eg at 25»C
 Vapor Deniityt  2.IS
 Flaah Pointi  -?7.i»c
 Vinyl chloride
 Page 1
 October 1985
Preceding page Wank

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Transport  and fate

     Volatilisation  from aquatic and terrestrial systems is
the most important transport process for distribution of vinyl
chloride throughout  the environment*  ialf-lives in aquatic
.systems range from several minutes to a few hours, depending
on temperature, water turbulence, and mixing affieiancy.  Photo-
oitdHtion  in -the  troposphere la tha dominant environmental
fate* of vinyl, chloride.  Vinyl chlocida caaeta rapidly with
hydroxyl radicala, forming hydrogan chlorida or formyl chlocida.
Formyl chlorida,  if  formed, rapidly dacompoaaa to ylald carbon
monoiida and hydrogan chlorida.  Vinyl chlorida in tha ataoaphara
la aipactad to be destroyed within ona or two daya of ita release.
Tha hydrogan chlorida fomad ia raportad to ba removed from
tha tropoaphara during praeipitation.

     Photolyaia doaa not appaar to ba an important fata process
in aquatic ayatama.  Furthermore, photooxidation daatroya vinyl
chlorida bafora it can raach tha stratoaphere, where diract photo-
lyaia could occur.   Baaad on available Information, hydrolysis,
aorptlon,  bioaccuaulation, and biodagradation do not appaar to.
ba important anvironmantal fata procasaaa.


laalth Bffacta

     IARC  conaidara  vinyl chlorida to ba a Category I human
carcinogen, cauaing  angioaarcomaa of the liver and tumors of
the brain* lung,  and heaolymphopoietic syatam ia humaas,  vinyl
chloride it carcinogenic in mice, rate, and hamatarsi it producea
tumors at  several sitea» including angioaarcomas of the liver,
after oral or Inhalation exposure,  vinyl chloride, both aa
a vapor and in aolution, is mutagenic in- aeveral biological
aaaay systems,  in addition, chromosome aberrations including
fragments, dicenties and rings, breaks, and gaps have been
found in workers  occupationally exposed to vinyl chloride.
The evidence en its  teratoganic and reproductive effects is
equivocal.  Minor skeletal abnormalities and increased fetal
death rates nave  been observed in the offspring of experimental
animals exposed by inhalation to vinyl chloride,  in humans,
a significant increase ia fetal deaths was seea in women whose
husbands were exposed to vinyl chloride.  Also, an excess number
of central nervous system disorders and deformities of the
upper alimentary  tract, genital organs, and feet were observed
in stillborn and  live children born in cities with vinyl chloride
facilities.  lowever, further research is necessary before
the link between  vinyl chloride and these observed effects
can be positively established.

     Acute occupational exposure to high concentrations of
vinyl chloride can produce symptoms of narcosis in humans.
Respiratory tract irritation, bronchitis, headache, irrits-


Vinyl chloride
Page 3
October If is                 <

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        ±ntan*G «jtposure  to  vinyl chloride  if associated with
 •ultiple  systeaic disorders,  including  a  sclerotic  syndrome,
 aero-osteolysis, throabocytopenia,  and  liver damage, eonaiBt-
 ing of damage  to partnchymal  calls,  fibrosis of  the livac cap-
 sule, periportal fibrosis aasociatad with hepatoaegaly , and
 aplenoaegaly.  Concentrations ancountarad by workara in indus-
 trial uiinf o< producing  vinyl chlorida ara raportadly quita
 variabla  and nay ranga  fcoa  lass than tha limit  of  da tact ion
 to eavaral grans par cubic aatar.

     Acuta inhalation axpoaura of axparimantal animals to high
 concentrations of vinyl chlorida can result in narcosis and
 death.  The 2-hour LC_0 value for rats  is 390 g/m .  Chronic
 exposure  of axpariaental  aniaals can result in growth disturbances
 and histopathologieal and histochenical lesions  in  the liver*
 kidneys,  spleen, and lungs.


 Toxicitv  to Wildlife and Domestic Aniaals

     Ho information is  available concerning tha  toxicity of
 vinyl chloride to domestic aniaals  or wildlife.


 Regulation and Standards

 fcnbient Water Quality Criteria (OS EPA) i

     Aquatic Lift

     Tha  available data art  not adequate  for establishing criteria.

     Baaan Health

     Estimates of tha carcinogenic  risks  associated with lifetime
     exposure to various  concentrations of  vinyl chloride in
     water ares

                                 Concentration

                                 20 ng/liter
                                 2.0 ttf/lltac
                                 0.2
CAS Onit ftitk  (OSZPA)i   1.75xlQ"2  (»f /kg/day)"1

OSHA standards i  26 ag/a? TWA
                 13 ag/mVlS ain Ceiling Level

ACGII Thraahold Liait Valuat  luaan  carcinogen 10 ag/a3
Vinyl chloride
faga 3
October 1185
                                                              aca*

-------
 REFEREMCES

 AMERICA* CONFERENCE Of  GOVERJIMENTAl,  INDUSTRIAL HYGIENISTS  (ACGII).
      1980.  Documentation of  the  Threshold Limit Values.   4th ed.
      Cincinnati,  Ohio.  488 pages

 INTERNATIONAL AGENCY FOR  RESEARCH ON CANCER  (IARC) .   1979.
      IMC Monographs on tht Evaluation of Carcinogenic Risk
      of Chemicals to Humana.  Vol. 19:  SOB* Monomers, Plastics
      and Synthetic Elastomers,  and Acrolein.  World Health
      Organization, Lyon,  Franc*.  Pp. 377-438

 NATIONAL INSTITUTE FOR  OCCUPATIONAL  SAFETY AND HEALTH  (NIOSH).
      1983.   Registry of Toxic Effects of Chemical  Substances.
      data Base.   Washington,  D.C. October 1913

 SAX,  H.I.   1175.   Dangerous Properties of Industrial Materials.
      4th ed.   Van Nostrand Reinhold  Co., Hew York.  1,258 pages

 O.S.  ENVIRONMENTAL PROTECTION AGENCY (USEPA).  1979.  Water-
      Related  Environmental Fate of 129 Priority Pollutants.
      Washington,  D.C.   December 1979.  ETA 440/4-79*029

 U.S.  ENVIRONMENTAL PROTECTION AGENCY {USEPA).  1980.  Aabient
      water  Quality Criteria for Vinyl Chloride.  Office of
      Water  Regulations  and Standards, Criteria and Standards
      Division, Washington,  B.C.  October 1910.  SPA 440/5-80-078

 D.S.  ENVIRONMENTAL PROTECTION AGENCY (USEPA),  1984.  Health
      Effects  Assessment foe Vinyl chloride.  Environmental
      Criteria and Assessment  Office, Cincinnati, Ohio.   September
      1984.  ECAO-CIN-H036  (Final Draft)

 U.S.  ENVIRONMENTAL PROTECTION AGENCY (USEPA}.  1985.  Health
      Assessment Document  for  Dichloroaethane  (Methylene Chloride).
      Office of Health and Environmental Assessment.  Washington,
      D.C.   February 1985.   SPA  600/8-82/004F

 WEAST,  R.E.,  ed.   1981.   Handbook of Chemistry and Physics.
      62nd  ed.  CJtC Press,  Cleveland, Ohio.  2,332  pages
Vinyl chloride
Page 4
October 1985
                                                                  J

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                                             XYLBIES
                     Xylene has been shown to be fetotoxic In rats and mict.
                In human*, exposure to high concentration* of lylene adversely
                affects the central nervous system and irritates th« mucous
                •eabranes.
                Background Information

                     Xylene has three isomers, o-» •-» and p-xylene.  These
                three generally have similar chemical and biologieal character*
                istics and therefore will be discussed together.

                CAS Number:  Mixed:     1330-20-7
                             m-Xylenet  108-38-3
                             o-Xylene:  95-47-6
                             p-Xylenet  106-42-3
                Chemical Formula:  CcB

                IDPAC Name:  Dime thy Ibenzene

                Important Synonyms and Trade Names:

                     Nixed *ylene:  Dime thy Ibenxene, xylol
                     m-Xylenet      1,3-Diaethylbenzene/ »-xylol
                     o-Xylene:      1,2-Dimethylbentene, o-xylol
                     p-»Xylene:      1/4-Dimethylbenxene , p-xylol


                Cheaieal and ?hy s ic al ? rope r ties

                Molecular Weight:  106.17

                Boiling folats  Mixed:     137-140'C
                                •-Xylene:  13f*C
                                o-Xylene:  144*C
                                p-Xylene:
                        foinfc*  »-Xyltn«s  -48'C
                                o-Xyl«nsi  -25-C
                                p- Xylene:   13"C

                Specific Gravity:  0.86

                Solubility In Hateci  X60 mg/littt at 2S»C
                Xylenes
                P«9« 1
                October 1985
j

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 Solubility in Organiea:   Soluble in alcohol,  ether*  and other
                          organic solvents

 Log Octanol/Water Partition Coefficient:   3

 Vapor  Pressure:   10  mm Hg at 2S*C

 Vapor  Densityi  3.7

 Plash  Point:   2S*C (closed cup}


 Transport  and Pate

     Volatilisation  and  subsequent photooxidation by reaction
 with hydroxyl radical* in tha atmosphere  art  probably important
 transport  and fata processes for xylene in tha uppar layer
 of  toil  and  in aquatic enviroiusents.   Products of tha hydroxyla-
 tion raaetion include  carbon dioxide,  peroxyacetylnitrate  (PAN),
 and ere sol.   Xylana  binda to aediaent  in  water and to organies
 in  aoila and  undergoes aicrobial degradation.   Biodegradation
 is  probably  the  scat important fate proceaa in both toils and
 the aquatic  environment.   Xylenes have been ahown to persist
 for up to  6 months in. soil.   Because of their lov water aolubil-
 ity and  rapid biodegradation, xylenes  are unlikely to leach
 into ground water in  high  concentrations.


 Health Effects

     Tha National Toxicology Prograa (HTP) is tasting xylene
 for carcinogenicity  by adminiatering it orally to rats and
 mice.  Although  the  results have not been finalized,  it. does
 not appear to be carcinogenic in rats.    Results  have not been
 reportad for  mice.   Xylene was not found  to be mutagenic in
 a battery  of  short*tern assays.   Xylene is not teratoganic
 but has  cauaed fetotoxicity in rats and1 aice.   Acute exposure
 to  rather  high levels  of  xylene  affecta the central nervous
 system and irritates the  mucous  aembranes.  There is limited
 evidence of effects  on other organ ays tarns, but.it was not
 possible to attribute  these  effects solely to xylane as other
 solvents were present.  The oral LDKn  value of xylene in rats
 is  5,000 ag/kg.                     90


 Toxicity to Wildlife and  Poaeatic Animals
^
     Xylene adversely  affected adult trout at concentrations
 as  low as  3.6 ag/litar in a continuous flow ayataa and trout
  .C. Eaatin, HTP Chemical Manager;  personal cosmunicatlon,  1984


Xylenes
Page 2
October 19S5

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 fry avoided xylene at concentrations greater than 0.lag/liter.
 The LC.Q value In adult trout was determined to be 13.$ mg/liter.
 LC.. vllues for other freshwater fish were around 30 ag/liter
 in3! static system, which probably underestimated toxicity,
 Only i few studies have been don* on tht toxicity of xylene
 to saltwater species.  These indicated that the •<- and o-xylene
 isomers probably have similar toxic it las and am probably less
 toiic than p-xylene, and that saltwater species are generally
 •ore susceptible than freshwater species to the detrimental
 effects of xylane (LC50 * 10 a§/liter for a- and o-xylene and
 LC.g * 2 ag/liter for p-xylene).  However, it should be stressed
 that these generalizations are based on limited data.

     Ho information on the toxieity of xylenes to terrestrial
 wildlife and domestic animals wa« available in the literature
 reviewed.  However, because of the low acute toxieity of xylenes
 it is unlikely that they would be toxic to wild or domestic
 birds and mammals.
Regulations and Standards

                          is  (air) i
                                    870 ng/m* 10-min Ceiling Level
NIOSH Recommended Standards (air) i  435 ag/m, TN&
                                    a?o ««/*•» ifl-n
OSHA Standard (air):  43S mg/m3
REFgREHCSS

NATIONAL INSTITUTE FOR OCCOPATTONAL SAFETY AND HEALTH  (NIOSH) .
    •1983.  Registry of Toxic Effects of Chemical Substances.
     Data. Base.  Washington, D.C.  October 1S83

NATIONAL RESEARCH COUNCIL  (HKC).  1980.  The Alkyl Benzenes.
     National Academy Press, Washington, D.C.

0,5. ENVIRONMENTAL PROTECTION AGENCY  (USEPA).  1978.   Initial
     Report of the TSCA Inter agency Testing Coma it tee  to the
     Administrator, Environmental Protection Agency.  January
     1978.  EPA Sf0-10-78/001

O.S. ENVIRONMENTAL PROTECTION AGENCY  (OSEPA).  1979.  Water-
     Related Bnvironaental Fate of 129 Priority Pollutants.
     Washington, D.C.  December 1979.  SPA 440/4-79-029

O.S. ENVIRONMENTAL PROTECTION AGENCY  (USEPA).  1984.  Health
     Effects Assessment for Xylene.  Final Draft.  Environmental
     Criteria and Assessment Office* Cincinnati, Ohio.   Sep-
     tember 1984.  BCAO-CIN-B006
Xylenes
Page 3
October 1985
                                                          Ammocmtmu

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 VERSCHUEREN,  K.   if??.   Handbook of Environmental  Oat* on Off
      Chaaicals.   Van  Host rand Rtinhold Co., !f*w York.  §59 pa

 WCA5T>  X.B.f  ad.   1911.  Handbook of Chtniitry  and fhyties.
      62nd  td.  CRC Pr«*i,  Cl«valand, Ohio.  2,332  pagaj
     4
October 1985

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                               IIIIC
Summary
     Xngestlon of excessive amounts of sine can cause £tv*r,
von It ing, and stomach cramps.  Zinc oxide fyiMJ can eaus* aetal
fuse fever*  Inhalation of aists or fumts may irritate tht
respiratory tract, and contact with sine chloride may irritate
the tyes and akin.  High levels of sine in the diet have been
shown  to retard growth and produce defective aineralixation
of bone.
Back ground Inforaation

     Zinc generally exists  in nature as  a salt with, a valence
of +2, although  it is also  found in four other stable valences.

CAS Number:  7440-66-6

Chemical Poraula:  Zn

IUPAC Name:  Zinc


Chemical and Physical Properties

Atonic Weight:   65.33

Boiling fointi   907*C

Melting Point:   419.58*C

Specific Gravity:  7.133 at 25*C

Solubility in Water*  Insoluble; aoae salts art soluble

Solubility in Organicsi  Soluble in aeid and alkali

Vapor Pressures  1 n Eg at 487*C


Transport and Fats-

     Zinc can occur in both, suspended and dissolved fora*.
Dissolved sine »ay occur 4s the free (hydrated) zinc ion  or
as dissolved complexes and  compounds with.varying degrees of
stability and toxicity.  Suspended  (undissolved) sine »ay be
dissolved following ainor changes in water caeaistry or Bay
b* sorbed to suspended Batter.  Th« predominant fate of tine
Sine
Page 1
October 1915

-------
 in aerobic aquatic systems is sorption of  the divalent cation
 by hydrous icon and manganese oxide*,  clay Minerals,  and  organic
 •aterial.   The efficiency of the**  material*  in removing  sine
 from  solution  varies according 60 their compositions  and  concen-
 trations;  the  pH and salinity of the water;  the concentrations
 of complexing  ligands;  and the concentration  of sine.  Concen-
 tration* of line In suspended and bad sediments always exceed
 concentrations in ambient water.   In reducing environments,
 precipitation  of xinc sulfide limiti the nobility of  sine.
 However, under aerobic  conditions,  precipitation of zinc  comp-
 ounds is probably important only where sine  is present in high
 concentrations.  Zinc tends to be more readily sorbed at  higher
 pH than lower  pi! and tends to be desorbed  from sediments  as
 salinity increases.  Compounds of zinc with the common ligands
 of surface waters are soluble in most neutral and acidic  solu-
 tions,  so  that zinc is  readily transported in most unpolluted,
 relatively organic-free waters*

      The relative mobility of line  in soil is determined  by
 the same factors affecting its transport in aquatic systems.
 Atmospheric transport of zinc is also possible.   However, except
 near  sources such as smelters» zinc concentrations in air are
 relatively low and fairly constant.

      Since it  is an essential nutrient, zinc  is strongly  bio-
 accumulated even in the absence of  abnormally high ambient
 concentrations.  Zinc does not appear  to be biomagnified.
 Although zinc  is actively bioaccumulated in aquatic systems,
 the biota  appear to represent a relatively minor link compared
 to the  sediments.   Zinc is one of the most important  metals
 in biological  systems.   Since it is actively  bioaecumulated,
 the environmental concentrations of zine probably exhibit, sea-
 sonal fluctuations*


 Health  Effects

      Testicular tumors  have been produced  in  rats and chickens
 when  zine  salts are injected intra-testicularly,  but not when
 other routes of administration are  used.   Zinc may be indirectly
 important  with regard to cancer  since its  presence seems  to
 be  necessary for the growth of tumors.   Laboratory studies
 suggest  that although zinc-deficient, animals  may be more  sus-
 ceptible to chemical induction of cancer,  tumor  growth.is slower
 in  these animals.   There is no evidence that  zinc deficiency
 has any  etiological role in human cancer.  There are  no data.
 available  to suggest that zine is mutagenic or teratogenie
 in  animals) or  humans.

      Zinc  is an essential trace element that  is involved  in
 enzyme functions*  protein synthesis,  and carbohydrate metabolism.
 Ingestion  of excessive  amounts of zinc may cause fever, vomiting,


 Zine
Page  2
October  Idas
                                                                   J

-------
 stomach  cramps,  and diarrhea.  Fuses of  freshly formed sine
 oxide  can  penetrate deep  into the alveoli and cause metal fume
 fever,   line oxide dust does not product this disorder.  Contact
 with sine  chloride can causa skin and eye irritation.  Inhalation
 of  mists or  fines ma/ irritate the  respiratory and gastrointes-
 tinal  tracts.  Sine in excess of 0.251 in the diet of rats
 causes growth  retardation, hypochromic anemia/ and defective
 mineralization of bon*.   No zinc toxicity is observed at dietary
 levels below 0.251.

     Studies with animals and humans indlcatt that metabolic
 changes  may occur due to  the interaction of zinc and other
 metals in  the  diet.  Exposure to cadmium can cause changes
 in  the distribution of zinc, with increases in the liver and
 kidneys, organs  where cadmium also  accumulates.  Sicessive
 intakt of  zinc may cause  copper deficiencies and result in
 anemia.  Interaction of zinc with iron or lead say also lead
 to  changes that  are not produced when the metals are ingested
 individually.


 Toxicity to Wildlife and  Somestic Animals

     Zinc produces acute  toxicity in freshwater organisms over
 a range  of concentrations from 90 to 58,100 ug/littr and appears
 to  be  less toxic in harder water.   Acute toxicity is similar
 for freshwater fish and invertebrates.   Chronic toxicity values
 range  from 4?  to §52 yg/liter and appear to be relatively unaf-
 fected by hardness.  A final acute-chronic ratio for freshwater
 species of 3.0 has been reported.   Although most freshwater
 plants appear  to be insensitive to  zinc, on* species, the alga
 Selenaatrun capricornutua, exhibited toxic effects at concen-
 trations from  30 to 700 ug/litar.   Reported acute toxicity
 values range from 2*730 to 13,000 ug/liter for saltwater fish
 and froa 166 to  55,000 ug/litar for invertebrate saltwater
 species.  Zinc produce* chronic toxicity in the mysid shrimp
 at  166 ng/littr.  The final acute-chronic ratio for saltwater
 species  is 3.0.  toxic effects art  observed in saltwater plant
 species  at line  concentrations of 50 to  25,000 jig/liter.  Bio-
 concentration  factors of  edible portion* of aquatic organisms
 range  froa 43  for the soft-shell elan to 16,700 for the oyster.

     Zinc poisoning has occurred In cattle.  la one outbreak,
 poisoning was  causad by food accidentally contaminated with
 zinc at * concentration of 20 g/kg.  An estimated intake of
 140 g of line  per cow per day for about  2 days was reported.
 The exposed cows exhibited severe enteritis, and some died
 or  bad to be/ slaughtered.  Postmortem finding! showed severe
 pulmonary emphysema with  changes la toe myocardium, kidneys,
 and liver.  Zinc concentrations In  the liver were extremely
 High.   Based on  relatively Halted  data, tea* researchers have
 •peculated that  exposure  to excessive amounts of sine aay


 Zinc
Page 3
October 1985

-------
 constitute • hazard  to horses.   Laboratory  studies and find
 In foals living near lead-tine  saelters  suggest  that  excess
 exposure to xine say product ton*  changes,  joint affliction.
 and laaeness.   In pigs given dietary  sine at concentrations
 greater than 1,000 ag/ltg,  decreased food intake  and weight
 gain were observed.   At dietary levels greater than 2,000 ag
 deaths occurred as soon as 2 weeks after exposure.  Severe
 gastrointestinal changes and brain damage,  both  of which wer
 accompanied by  hemorrhage*,  were observed,  as well as  change:
 in the joints.   High concentrations of zinc were found in th
 liver.
 Regulations  and  Standards

 Ambient Water  Quality Criteria  (OSEPA)j

      Aquatic Life

      Freshwater

          Acute  toxieit*,   t(O.I3tln(hardness)J «. l.»s> ||f/Ut(
          Chronic  toxieitys   47  ug/liter

      Saltwater

          Acute  toxieityt   170 yg/liter
          Chronic  toxieity*   58  ug/liter

      Huaan Health

      Organoleptic  criterion:  S  »g/liter

 Secondary Drinking Water Standards   S Big/liter

 MIOSH Recomaended  Standard!   S »g/»3  (sine oxide)

 OSHA  Standards  S  »g/a3 TWA (sine oxide)

 ACGIH Threahold  LUit Values:

      Zinc chloride fuaei i  »g/«  TWA

                         2  «g/»  ST2L
     Sine oxide fuses     S mg/m* TWA
                          10 »g/«3 STEL
     Sine oxide dusts    10 »g/»3 TWA  (nuisance ^articulate)

     Zinc stearatei      10 «g/a3 TWA  (nuisance psrticulate)

                         20 »g/»3 STEL
Zinc
Page 4
October 1985

-------
AMERICAN CONFERENCE Of GOVERNMENTAL IHDUST»IAL BYGIENXSTS (ACGIH) .
      1980.  Documentation of the Threshold Limit Value*.  4th
      •d.  Cincinnati, Ohio.  418 pages

CASARETT, 1.3., and DOOLL, J., eds.  1975.  fa*icolofyt  Tht
      Basic Science of Poisons.  Maemillan Publishing Co.* N«w
      York.  768 page*

NATIONAL INSTITUTE FOR OCCUPATIONAL SAFETY AND HEALTH  (NIOSH) .
      1983.  Registry of Toxic Effects of Chemical Substances.
      Data Base.  Washington, D.C.  October 1983

SAX,  H.I,  1975.  Dangerous Properties of Industrial Materials.
      4th ed.   Van Hostrand Reinhold Co., New York.  1,253 pages

O.S.  ENVIRONMENTAL PROTECTION AGENCY (USEPA).  1979.  Water-
      Related Environmental Fate of 129 Priority Pollutants.
      Washington, D.C.  December 1979.  EPA 440/4-79-029

U.S.  ENVIRONMENTAL PROTECTION AGENCY (OSEPA).  1980.  Ambient
      Water Quality Criteria for Zinc.  Office of Hater Quality
      and Standards, Criteria and Standards Division, Washington,
      D.C.  October 1980.  EPA 440/5-80-079

O.S.  ENVIRONMENTAL PROTECTION AGENCY (USEPA).  1984.  Health
      Effects Assessment for Zinc.  Final Draft.  Envirenaental
      Criteria  and Assessment Office, Cincinnati, Ohio.   Sep-
      tember 1984.  ECAO-CIN-H048

O.S.  ENVIRONMENTAL PROTECTION AGENCY (OSEPA).  1985.  Wealth.
      Assessment Document for Dichloromethane (Metnylene Chloride).
      Office of Health and Environmental Assessment.  Washington,
      D.C.  February 1985.  EPA €00/8-82/004?

WEAST, R.E., ed.  1981.  landboofc of Chemistry and Physics.
      62nd ed.  CRC Press, Cleveland, Ohio.  2,332 page*
Zinc
Page 5
October 1985

-------

-------
                                      INDBX
Preceding page blank

-------

-------
    CHEMICAL NAME/
    SYNONYM/TRADE NAME
       LISTED UNDER THE
       FOLLOWING CHEMICAL MAKE
    Acenaphthene
    Acenaphthylene
    Acetic acid
    Acetic ethec
    Acetone
    Acetylene tetrachloride
    trans-Acetylene dichloride
    Acrolein
    Acrylaldehyde
    Acrylonitrile
    Acrylic aldehyde
    Agroteet

    Altar
    Aldrin
    AlJcanes
    Alkyl benzenes
    Allylaldehyde
    2-Aainoethanol
    Anthracene
    Antimony
    Antimony trioxide
    Aroclor
    Arsenic
    Asbestos
    Asex
    Atlacide
    Attac
    Barium
    1,2-Benzanthracene
       Acenaphthene
       Acenaphthylene
       Acetic acid
       Ethyl acetate
       Acetone
       1,1,2,2-Tetrachloroethane
       1i2-trani-Dichloroethylene
       Acrolein
       Acrolein
       Acrylonitrile
       Acrolein
       2,4-Dichlorophenoxyacetic
          acid
       Chlorobenxilate
       Aldrin/Dieldrin
       Alkanet
       Alkyl benzenes
       Acrolein
       Etbanolamine
       Anthracene
       Antimony
       Antimony
       Polychlorinated biphenyls
       Arsenic
       Asbestos
       Sodiua chlorate
       Sodiua chlorate
       Toxaphene
       Bariua
       Benzo(•)anthracene
                                                        .Clement AMoo
vPreceding page blank
s*£

-------
 CHEMICAL NAME/
 SYNONYM/TRADE NAME
LISTED UNDER THE
FOLLOWING CHEMICAL NAME
 Benzabar

 Benzac

 Benzene
 Benzene chloride
 Benzene hexachloride
 Benzene tetrachloride
 o-Benzenedicarboxylic acid
 Benzidine
 Benzilan
 Benzo(a)anthracene
 Benz (b)phenanthrene
 Benz(a)phenanthrene
 2 f 3-Benzophenanthrene
 Benzosulfonaxole
 Benzothiazole
 Beryllium
 BHC
 Bibenzyl
 bia(2-Hydroxyethyl)ether
 Brushtox

 Butanol
Butyl alcohol
Butanone
C-46
Cadmiun
Caatphechlor
2,3,6-Trichlorobenzoic
   acid
2,3,6-Trichlorobenzoic
   acid
Benzene
Chlorobenzene
Heaachlorocyclohcxane
1* 2,4,5-Tetrachlorobenzene
n-Dioctyl phthalate
Benzidine
Chlorobenzilate
Benzo(a)anthracene
Benzo(a)anthracene.
Chrysene
Benzo(a)anthracene
Benzothiazole
Benzothiazole
Beryllium
Hexachlorocyclohexane
Oiphenylethane
Diethylene glycol
2,4,5-Trichlorophenoxy-
   acetic acid
Butanol
Butanol
Methyl ethyl Ketone
Heiachlorobutadiene
Cadaiua
Toxaphene

-------
CHEMICAL NAME/
SYNONYM/TRADE HAMS
LISTED UNDER THE
FOLLOWING CHEMICAL HAME
Carbide  6-12
Carbon hexachloride
Carbon tetrachloride
Cellulose nitrate
Cellulose tetranitrate
Chlorate of soda
Chlorate salt
Chlordane
Chlorax
Chlorinated caraphene
Chlorine
Chlorob*nz«n*
Chlorobenzilate
p-Chloro-m-cresol
Chloroethane
Chloroeth«n«
lf-Chloro-2-(bet«-chloro-
  ethoxy) ethane
bi s { 2-Chloroethoxy) e thane
bis (2-chloro«thyl) ether)
Chloroethylene
Chloroform
Ch lor one thane
Chloro-a-nitrob«nx«n«
l-Chloro-3-nitrob«n2«n«
Chlorophenothan*
Chlorothene
Chromic acid
Chromium
Ethyl hexanediol
Hexachloroethane
Carbon tetrachloride
Nitrocelluloae
Nitrocellulose
Sodium chlorate
Sodium chlorate
Chlordane
Sodium chlorate
Toxaphene
Chlorine
Chlorobeniene
Chlorobenzilate
p-Chloro-m-creaol
Chloroethane
Vinyl chloride
bis(2-Chloroethyl)ether

bis(2-Chloroethoxy)ethane
bis{2-chloroethyl}ether
Vinyl chloride
Chloroform
p-Chloro-m-cresol
Methyl chloride
p-Chloro-m-cresol
l-Chloro-3-nitrob«nzent
l-Chloro-3-nitrobenzene
DOT
1,1,1-Trichloroethane
Chromium
Chromium
                                                 o

-------
 CHEMICAL NAME/
 SYNONYM/TRADE  NAME
LISTED UNDER THE
FOLLOWING CHEMICAL HAME
 Chryiene
 Cfflpd  $-12  Insect Repellant
 Cobalt
 Collodon
 Copper
 Cresol
 Cuaene
 Cyanide
 Cyanoethylene
 Cyanuric acid
 Cresylle add
 2,4-D

 DBCP
 Dd
 1,1-DCE
 2,4-DCP
 ODD
 DOE
 DDT
 Creaylic acid
wetd Brush Killer

DEEP
 414f-Diaainobiphenyl
DllMtnzyl
Dibromochloropropan*
 2,3-Dibr ooo-1-ptopanol
   phosphat*
 1,2-Dichlocobenztn«
Chrysene
Ethyl hexanediol
Cobalt
Nitrocellulose
Copper
Creaol
Alkyl benzenes
Cyanide
Acrylonitrile
Cyanuric acid
2,4-Dinethylphenol
2,4-Dichlorophenoxyacetic
   acid
Dibroaochloropropane
Dichlorobenzenes
1,1-Dichloroethylene
2 f 4-Dichlorophenol
out
DOT
DOT
Creaol
2 f 415-Tr i colorophenoxy-
   acetic acid
bii(2-Ethylhexyl)phthaiate
Benzidine
Diphenylethane
Dibroaochloropropane
Tri»(2,3-Dibromopropyl)
   phoapbate
Dichlorobenzenes

-------
 CHEMICAL  NAME/
 SYNONYM/TRACE  SAME
LISTED UNDER THE
FOLLOWING CHEMICAL HAMS
 1,3-Dichlorobenzene
 Dichloro-2,2-dichloroethane
 Dichlorodiphenyltrichloroethane
 1,1-Dichloroethane
 1,2-Dichloroethane
 1,l-Dichlorocthen«
 2,2'-Dichloroethyl ether
 111-D i chloro* thylene
 1,2-trans-Dicbloro«thylen«
 Dichloromethane
 2,4-Dichlorophenol
 2,4-Dichlorophenoxyacetic acid

 1,2-Dichioropropan«
 It 3-Dichloroprop«n«
 lf 3-Dichloropropyl«n«
 Dicofol
 Oicot«xt

 Di«ldrin
 Ditthyl t>«nztn«
 1,4-Oiethylentdioxyd«
 Diethylen« glycol
 Diethyl oxid«
 Diethyl •sttc phthalic acid
 Diethyl ether
 Diethyl oxide
Ditthyl phthalate
 1,2-Dihydroxy ethane
Diiaobutyl ketone
Dlchlorobenzenes
1,1,2/2-Tetrachloroethane
DDT
1,1-Dichloroethane
1,2-Dichloroethane
1il-Dichloto«thylen«
bi s(2-Chloroethyl)t th«r
1,1-Dichloroethylene
It2-tran«-Dichloroethylene
Hethylene chloride
2,4-Dichlorophenol
2,4-Dichlorophenoxyacetic
   acid
1,2-Dichloropropane
1,3-Dichloropropene
If 3-Dichloropropene
Dicofol
2,4-Dichlorophenoxyacetic
   *cid
Aldrin/Dieldrin
Alky! benzenea
1,4-Dioxane
Diethylene glycol
Tetrahydrofuran
Diethyl phthalate
Ethyl ether
Ethyl ether
Ditthyl phthalate
Ethylene glycol
Diiaobutyl ketone
                                                            «oci«c«a

-------
 CHEMICAL NAME/
 SYNONYM/TRADE IAMB
LISTED UNDER THE
FOLLOWING CHEMICAL KANE
 Dinethylaminoethyl methacrylat*
 Dicophane
 2-Din*thylaaiinoethyl-2-
    methylpropenoate
 Dimethylaniline
 D imethylbenzene
 2i6-Dimethyl-4-hepatanone
 Dimethyl  daton*
 2,4-Dimethyl-l-hydroxybenzen*
 Dim«thylnitro«aain*
 2 f 4-Dlfflethylph«nol
 Dimethylphenylamine
 n-Dioctyl phthalat*
 Dioform
 li 4-Dioxan*
 Dioxin

 Dioxins

 Diphenyl«than«
 Diphenyl «th«r
 Diphenyl oxid«
Di{2-«thylh«xyl)pbth«l»t«
OHM
DMNA
Dolan
009
Dowicid* S
Dowicide 7
Durana
Durotox
Dimethylaminoethyl methacrylate
DDT
Dimethylaminoethyl methacrylate

Dimethylaniline
Xylenes
Diiaobutyl keton*
Acetone
2i4-Dinathylphenol
Diaethylnitroaaaine
2,4-Dimethylphenol
D imathylanilina
n-Dioctyl phthalate
1,2-trana-Dichloroathylen*
1,4-Dioxana
2,3,7,8-tatr«chlorodibenzo-
  P-dioxin
Polychlorinated dibenzo-
   p-dioxin
Diphanylathane
Phanyl ether
Phenyl ether
bii(2-Ethylhexyl)phthalate
Diaiethylnitroaafflin*
Dimethylnitroaamine
Haxachlorobutadiane
n-Dioctyl phthalate
2,4,5-Trichlorophenol
Pan tichlorophanol
Alkyl b«nzana«
Pantachlorophenol

-------
CHEMICAL NAME/
SYNONYM/TRADE NAME
LISTED UNDER THE
FOLLOWING CHEMICAL NAME
End;in
Endrex
1,2-Ethanediol
Ethan*  trichloride
Ethanol
Ethanolanine
bis(2-chloroethyl) Ether
Sthoxyethane
Ethyl acetat*
Ethyl alcohol
Ethylbeniene
Ethylbenzol
Ethyl chloride
Ethyl-4,4-dichlorobenzilite
Ethylane alcohol
Ethylene dichloride
Ethylene dlglycol
Ethylene glycol
Ethylene hexachloride
Ethylene trichloride
Ethyl ethanoate
Ethyl ether
Ethyl hexanediol
Ethyl hexylene glycol
Ethyl aethyl feetone
bis U-ethylneiyl)phthalat*
di{2-ethylhexyl)phthalate
Ethylidine chloride
Ethylidene dichloride
2-Bthyl-3-propy1-1,3-
   propanediol
Endrin
Endrin
Ethylene glycol
1,1,2-Trichloroethane
Ethanol
EthanolanIne
bia(2-chloroethyl)  Ethec
Ethyl ether
Ethyl acetate
Ethanol
Ethyl benzene
Ethyl benzene
Chloroethane
Chlorobenzilate
Ethylene glycol
I* 2-Dichloroethan*
Ethylene glycol
Ethylene glycol
Hexachloroethane
Ttichloroethylene
Ethyl acetate
Ethyl ether
Ethyl hexanediol
Ethyl hexanediol
Methyl ethyl fcetone
bi 8{2-ethylhexyl)phthalate
bis{2-ethylhexyl)phthalate
1,1-Dichloroethane
1,1-Dichloroethane
Ethyl hexanediol

-------
 CHEMICAL  NAME/
 SYNONYM/TRADE NAME
LISTED UNDER THE
FOLLOWING CHEMICAL NAME
 Ftnopeop

 Fluoranthene
 Fluorocarbon  11
 Fluorotrichloromethane
 Folbex
 Focaaldehyd*
 Formalin
 Freon-11
 Funszone
 Gesarol
 Glyeol
 Glyeol Oichloridt
 Glyeol ethyient ethtr
 Grain alcohol
 HCB
 HCBD
 HCB
 Hemimellitin*
 Heptachlor
 Heptant
 Hexachlorobeni«nt
 H«xachlorobut*di«n«
 Bflxaehlococyelohtian*
 Hexachloro«than«
 Hexachloro«thyl«n«
 Hexachloroph«n«
Hexan«
2,4,5-Trichlorophenoxy
   acetic acid
FluoEanth«n*
TrichloroCluoromethan*
TrichloroCluoromcthane
Chlorob«ntilat*
Formaldehyde
Formaldehyde
Trichlorofluoromethane
Dibromochloropropane
DDT
Ethylene flycol
1t2-Dichloroethane
1,4-Dioxane
Ethanol
Hexachlorobeniene
Hexachlorobutadiene
Hexachlorocyclohexane
Alkyl b«nzen««
Heptachlor
Alkane»
Bexachlorobenzene
Hexachlorobutadiene
Hexachlor ocyclohexane
Hexachloroethane
Hexachloroethane
Hexachlorophene
Hexane
Hexachlorophane
       iiobutyl ketone
                                8
                                                                      I

-------
 CHEMICAL  SAME/
 SYNONYM/THADE NAME
LISTED UNDER THE
FOLLOWING CHEMICAL NAME
 beta-Hydroiyethylamine
 2-Hydroxyni trolbenzene
 Iron
 Isobutanol
 Isobutyl  alcohol
 Isobutyl  ketone
 Isobutyl  methyl ketone
 Isocyanuric acid
 Isodurene
 2-Isopropoxypropan«
 Isopropyl acetone
 Isopropyl benzene
 Isopcopyl ether
 Kanechlor
 Kelthane
 Xlortx
 Kuran

 Kusatol
 Lead
 Lindane
 Lithium
 Hagneslua
 Manganese
 n-chloronitrobenxene
HEX
Hendrin
Mercury
Mtsitylene
Metaphor
Methacrylate
Ethanolamine
2-Hitrophenol
Iron
Isobutyl alcohol
Isobutyl alcohol
Diisobutyl ketone  0
Methyl isobutyl katone
Cyanucic acid
Alkyl benzenes
Isopropyl ether
Methyl iaobutyl ketone
Alkyl benzenes
Isopropyl ether
Polycblorinated biphenyls
Dicofol
Sodiun chlorate
2,4,5-Tri chlorophenoxy
   acetic acid
Sodiun chlorate
Lead
Hexachlorocyclohexane
Lithium
Magnesiua
Manganese
l-Chloro-3-nitrobenzene
Methyl ethyl ketone
Endrin
Mercury
Alkyl benzenes
Methyl parathion
Mtthactylic acid

-------
CHEMICAL  NAME/
SYNONYM/TRADE NAME
LISTED UNDER THE
FOLLOWING CHEMICAL NAME
Methacrylie  acid
Methacrylic  acid, ntthyl aster
Methanal
Methanecarboxylic acid
Methane dichlorid*
Methanol
Methyiacrylic  acid
Methyl alcohol
Methyl benzene
Methyl chloride
Methyl chloroform
2-Methyl dodecane
3-Methyl hexane
2-Methyl pan tana
3-Methyl p«ntan«
2-Methyl tetradecane
2-Methyl tridecane
2,2-Methylene-bis(3,4,6-
   t r ichlorophenol)
Methylena chloride
Methylene dicblorida
Methyl ethyl beniene
Methyl ethyl Itetone
Ntthyl isobutyl ketone
Methyl methacrylata
Methyl-2-aethyl-2-prop«noatl.a
Methyl pacathion
4-Mathyl-2-p«ntanon«
Methacrylic acid
Methacrylic acid
Pornaldehyde
Acetic acid
Methylene chloride
Methanol
Methacrylic acid
Methanol
Toluene
Methyl chloride
1,1rl-Trichloroethane
Alkanea
Allcanea
Alkanes
Alkanea
Alkanas
Alkanes
Hexachlorophene

Methylene chloride
Methylene chloride
Ethyl toluene
Methyl ethyl ketone
Methyl iaobutyl ketone
Methacryllic acid
Methacryllic acid
Methyl par a til ion
Methyl iaobutyl ketone
                                10

-------
 CHEMICAL NANS/
 SYNONYM/TRADE HAKE
LISTED UNDER THE
FOLLOWING CHEMICAL NAME
 2-Methyl  propanol
 2-Methyl-2-propenoate
 MIBK
 MIX
 Mitlgan
 Monochlorobenzane
 Monochloroethane
 Monochloroethylene
 Monochloronethane
 Monoethanolaaine
 Moth  balls
 Nabac
 Naphthalene
 Naphthene
 NDMA
 Nemagon
 Heocid
 Nickel
 Nitrocellulose
 Nitrochlotobenztn*
 Nitro cotton
 2-Nitrophenol
 Nitrosodimethylaain*
 n-Methyl-n-nitroionethanamine
 n-Nitrosodi««thyl*ain«
 N,N-Dimethylb«nz«n«anin«  ^
 n,n-diaethylnitroa«ain«
 N-phenyldimethylaaine
Octyl phthalate
 Orthophoaphoric acid
 l,l'-0jcybis(2-chloroethane)
laobutyl alcohol
Methacrylic acid
Methyl isobutyl ketone
Methyl isobutyl ketone
Dicofol
Chlorobenzene
Chloroethane
Vinyl chloride
Methyl chloride
Ethanolamine
Naphthalene
Hexachlorophene
Naphthalene
Naphthalene
Dimethylni trotamine
D i b romochlor opr opane
DOT
Nickel
Nitrocellulose
l-Chloro-3-nitrobenzene
Nitrocellulose
2-Nitrophenol
Dimethylnitrosamine
Dinethylnitroiaaine
Dimethylnitrosamine
Dimethylaniline
Dimethylni trosaaine
Dimethylaniline
n-Dioctyl phthalate
Phosphoric acid
bis(2-Chloro«thyl) ether
                                11

-------
 CHEMICAL RAMS/
 SYNONYM/TRADE  NAME
LISTED UNDER THE
FOLLOWING CHEMICAL RAM!
 2 f2-Oxyd1ethanol
 PAR

 Paranaphthalene
 PCS
 PCDD

 PCI
 PCP
 s-Dio*ane
 Pefalan
 Pentachlorophenol
 Pentadecane
 Perchlorobenzene
 Perchlorobutadiene
 Percoloroethylene
 Perchloroaethane
 Phenacide
 Ph«nanthr«n«
 Phenol
 Phenol trinitrtte
 Phenox

 Phenoxyb«n»«n«
 Phenyl chloride
 Phenyldiaethylaaine
 Phenyleth«n«
Phenyl ether
Phenylaethane
Phosphoric acid
Phosphorus (white)
Diethylene glycol
Polycyclic aromatic
   hydrocarbons
Anthacene
Polychlorinated biphenyls
Polychlorintted dibenzo-
   p-dtoxins
Tetrachloroethylene
Pentachlorophenol
1,4-Dioxane
Methacrylic acid
Pentachlorophenol
Alkanes
Hexaehlorobenzene
He xachlor obut adIene
Tetrachloroethylene
Carbon tetrachloride
Toxaphene
Phenanthrene
Phenol
Picric acid
2,4-Dichlorophenoxyacetic
   acid
Phenyl ether
Chlorobentene
Oiaethylaniline
Alkyl benzenes
Phenyl ether
Toluene
Phosphoric acid
Phosphorus (white)
                                12

-------
CHEMICAL HAKE/
SYMONYM/TRADE RAMS
tISTID UHDEI THE
FOLLOWING CHEMICAL NAME
bU(2-*thylh**yl) Phthalat*
Picric acid
PSA

Pol/chlorinated biphcnyls
Polychlorinated dib«nzo-
   p-dioxin
Polycyclic aromatic
   hydrocarbons
Polynuclear aromatic
   hydrocarbons
Preventol
Propanon*
2-Prop«nal
Prop«r*nitrll*
2-Prop«nenitrilt
2-Prop«n-l-on*
Propyl carbinol
Propyl«n«chlor i d«
Propyl«n«dichlorld«
Pseudocuman*
Rat Rip
Rutf*rs 6-12
Selaniua
Sil7«r
Silvtr

Soda chlorat*
Sodiua
Sodium chlorate
Solublt fun cotton
bis(2-«thylhexyl) Phthalate
fierlc acli
Polycyclic aromatic
    hydrocarbons
Polychlorlnat«d biphenyla
Polychlorlnated dlbenzo-
   p-dloxin
Polycyclic aromatic
    hydrocarbons
Polycyclic aromatic
    hydrocarbons
2,4,5-TrIchlorophenol
Ac*ton*
Acrolain
Acrylonitrila
Acrylonitrila
Acroltin
1-Butanol
I,2-Dichloropropane
1,2-Dichloropropan«
Alkyl b«nx*n*«
Phosphorus (whit*)
Ethyl h««an«diol
S«l«niia
Silv«r
2,4,5-Trichlorophenoxy
   propionlc acid
Sodium ehlorat*
Sodiua
Sodiua chlorate
flitcoctllulos*
                                13
                                                            macia

-------
 CHEMICAL HAKE/
 SYHQHTfM/TRAOE
LISTED BNDER THE
FOLLOWING CHEMICAL NAME
 Stoddard  solvent
 Strobane-T
 Sym-triazinetriol
 2,4, 5-T

 Tar  camphor
 2,3,6-TiA
TCI
TCE
TCOO

TCPPA

TEL
Ttlone
1,2,4, 5-Tetrachlorobenzene
2,3/7, S~Tetraehiorodiben*o
  p-dioxin
1 t I i 2 t 2-Tt tracblorotthtnt
Tetrachloro«th«n«
Tetrachlorothyl«n«
Tttrachlorcai«than«
Tatradioxin
T«tra«thyi
T»tr««thyl pluaban*
Tttrahydrofuran
Tttraaethyl b«nx«n«
Tttraaethyl*n« ox id*
Thallium
Stoddard solvent
Toxaphene
Cyanurlc acid
2,4,I-Trlchlocophenoxy-
   acetic acid
Naphthalene
2,3,6-Trichlobenzoic
   acid
1,1,1-Tri chloroethane
Triehlorebenzene
Trichloroethylen*
2,3,7,i-Tetrachlorodibento-
  p-dtoxin
2,4,5-Trichlorophenoxy
   propionic acid
Tttraethyl lead
1,3-Dichloropropene
1,2,4,5-Tetrachlorobenzene
2,3,7,8-Tetrachlorodibenro-
  p-dioxin
1,1,2,2-Tetrachloroethane
Tetrachlorothylene
Tetrachlorothylene
Carbon tetrachloride
2,3,7,8-Tetrachlorodibenzo-
  p-dioxin
Tttraethyl lead
Tetracthyl lead
Tetrahydrofuran
Alkyl benxenes
Tetrahydrofuran
Thalliua
                                14

-------
CHEMICAL NAMZ/
SYNONYM/TRADE HAMS
LISTED UNDER THE
FOLLOWING CHEMICAL NAK2
 l-Thia-3-azaindene
 Titanium
 Toluene
 Toluol
 Toxaphene
 2,4,5-TP

 l»3,5-Triazine-2»4f*
   (lH,3H,5H)-trlon«
 Trichlorobenzene
 2,3, 6-Trichlorobenzoic acid

 1,1, 1-Tr ichloroethane
 l,l,2-Trichloro«th*n«
Trichloroethene
Tr i chloroethylen*
Trichlorofluoromethane
Trichlorotn«than«
 2,4, 5-Tr i chloroph«nol
 2 1 4 » 5-Tr i chloroph«no«y-
   acetic acid
2, 4, 5-Trichloroph«noxy
   propionic acid
Tricrtsol
Tri cyanic acid
Triethyl«n« glycol dichloride
Triglycol dichlocld*
Trihydroxycyanidin«
Benzothiazol*
Titanium
Toluene
Toluene
Toxaphene
2,4,5-Trichloroph«noxy
   propionic acid
Cyanuric acid

Trichlorobenzene
2,3,6-Trichlorobenzoic
   acid
1«1,1-Trichloroethane
1,1,2-Trichloroethane
Trichloroethylene
Trichloroethylene
Trichlorofluoronethane
Chloroform
2,4,5-Trichlorophenol
2,4,5-Tri chlorophenoxy
   acetic acid
2,4,5-Trichlorophenoxy
   propionic acid
Cresol
Cyanuric acid
bi«(2-Chloroethoxy)ethane
bin(2-Chloroethoxy)ethane
Cyanuric acid
Cyanuric acid
   trlaiina
                                IS
               Clemene Ammo&atmm

-------
 CHEMICAL (UNI/
 SYNONYM/TRADE NANS
LISTED UNDER THE
FOLLOWING CHEMICAL NAME
 Trlmethyl  benzene
 2»4»6-TrIn11 r ophenol
 THIS

 Tris(2,3-Dibromopropyl)
   phosphate
 Tris(2,3-1bromopropyl)
   phosphoric acid  eater
 Tryaben

 Undecane
 Vanadium
 Vinegar acid
 Vinegar naphtha
 VC
 VDC
 Vinyl chloride
 Weedar

 fallow Phoaphorua
 Vinyl cyanida
Vinylidana chloride
Vinyl trichloride
Wofatox
wood alcohol
Xylene
 2,4-Xylenol
Xylol
Zinc
Alfcyl benzenea
Picric acid
Tris(2,3-Dibromopropyl)
   phosphate
Trla(213-Dibromopropyl)
   phoaphate
Tria(2,3-dibromopropyl)
   phoaphate
2,3,S-Trichlorobenzoic
   acid
Alkanea
Vanadiua
Acetic acid
Ethyl acetate
Vinyl chloride
1f1-Dichloroethylene
vinyl chloride
2 f 4 r 5-Tr i chlorophenoxy-
   acetic acid
Phoaphorua (white)
Acrylonitrile
1,1-Dichloroethylene
1,1,2-Tr ichloroathane
Methyl parathion
Methanol
Xylene
2,4-Di»ethylphenol
Xylene
Sine
                                If


-------
                            APPENDIX A
                         HAZARD CRITERIA

     It is usually difficult to give a simple yes or no answer
to the question of whether or not a chemical is hazardous because
in most cases, gradations exist in such things as the quality
of data or species-specificity of the effects,  in addition,
the degree of hazard posed by a chemical depends on the dose
or environmental concentration and on the duration and other
circumstances of exposure.  In order to provide a dichotomous
response in these cases, it is necessary to determine general
criteria for classifying chemicals as having specific toxicity.
The criteria used in this system for determining whether a
chemical poses a particular type of hazard ace outlined below.

Carcinogenicity
     A compound is classified as a carcinogenic if it is a
known or suspected human carcinogen, if it has been shown to
be carcinogenic at a particular site in more than one species
or sex in an animal bioassay, or if it has been shown to increase
the incidence of site-specific malignant tumors in a single
species or sex, and there is a statistically significant dose*
response relationship in more than one exposed group.  Obser-
vations such ai site of application tumors in a skin painting
study or sporadic significant results in a bioassay will not
be considered indications of earcinogenicity unless supported
by other evidence.

-------
              To* tcity/Teratoqenicit
     Chemicals  ar«  classified  is  teratogens  and  reproductive
 toxins If  there is  suggestive  evidence  of  an effect  in  humans
 or  if  at least  on*  study  in whole animals  is clearly positive.
 Unsupported  in  vitro  evidence  is  considered  sufficient  to  clas-
 sify a chemical as  a  reproductive toxicity/teratogenieity  hazard.
     A chemical  is classified  as mutagenic  if  it has  given
a positive  result in at least  one of  the mammalian  in vivo
or bacterial or  mammalian cell in vitro assays  for  mutagen-
icity.  However, negative studies will be considered* and in
some cases  nay outweigh a weak positive response.
Acute Toxicity
     A compound  will be considered  to be acutely toxic  if it
has an oral LDjg <, 100 ag/kg,  an inhalation LC.~ <,  400  ng/ra3,
or a dermal L05Q <. 400
Chronic Toxicity
     Chemicals will be considered to cause chronic toxicity
if they caus* serious irreversible effects other than cancer
or reproductive effects after extended exposure to oral doses
of less than 180 »g/ kg/day, inhalation concentrations less
than 400 mg/m , or dermal doses less than 400 ag/kg/day.
                           v
Domestic Animal Toxicitv
     A chemical will be considered to be toxic to domestic
animals if a demonstrated serious toxic effect has been seen
in the field.  Also, chemicals that cause reproductive toxicity,
                                                                     J

-------
teratogenicity, or subchronic toxlclty at oral doses of less
than 100 mg/kg/day will be considered as domestic animal hazards
unless they are unlikely to be present at toxic levels off site.
E n v ir onmen t a1 To xie t ty
     A chemical is classified as hazardous to aquatic wildlife
if an acute LC-Q value in aquatic organisms is less than 1000
liter, or if the chemical has chronic effects at less than
100 M9/liter.
     A chemical is classified as hazardous to terrestrial wild-
life if toxicity haa been seen in the field or if the chemical
is acutely toxic or causes reproductive toxicity/teratogenicity
to representative species at oral doses less than 100 ng/kg
body weight.
     Chemicals that are persistent in the environment and that
are toxic at levels up to 10 times less than those indicated
above, are also classified as hazardous to the environment.

-------
HAZARD CLASSIFICATION
Chaaical.
Acenaphthene
Acenaph thy l*ne
Ac«tlc acid
Acetone
Accoleln
AcrylonltEile
Aldiin
Alkane*
Alkyl bencene*
Anthracene
Antiaony
Arsenic
Asb«atoa
Bar ilia
CAS MiMb*r
83-32-9
206-96-1
64-W-7
67-64-1
107-02-8
Wf-13-1
JOft-00-2


120-12-7
7440-K-0
7440-38-2
1332-21-4
7440-3f-J
Hazard
DcxMStlc Env iron-
Care ino- Keproductlve/ Nut«g«n- Acute Chronic Aniaal ntntal
genicity Teratogeniclty iclty Toxic ity Effect Toxicity Toxic ity




I X
• X XX
X X XX X XX

*
X
XX X
I XX XXX
x x
X X

-------
Hazard
Doaeatic Envii
Carcino- Reproductive/ Mutagen- Acute Chronic Animal Mnti
Chemical CAS MtiBber genlcity Teratogen icily icily Ton icily Effect Ton icily Toxic
Beniene
Bens id In*
Beoso(a) anthracene
B*nso(a)perylen«
Benso(«)pycen«
Ben so (k) Cluoranthene
Bensotb iaxole
Berylliim
g.-.-8i*C (lindan.)
1-Butanol
dl-n-Butyl phthalate
C-dalu.
Carbon tetrachloride
Chlordane
Chlorine
71-4J-2
92-87-5 X
5*- 55- 3 X
191-24-2
50-32-8 X
2Q7-08-9
95-W-9
7440-41-7 X
58-89-9 X
71-18-3
84-74-2
7440-43-9 X
56-23-5 X
57-74-9 X
7782-50-5
XX X
X X
X
X
X X
,

X X
XX X X

X X
X XXX
X
XX X X
X X

-------
Chmlcal
Cblorobeniene
Ch loroben* i 1 «t«
Chloroeth*ne
bic (2-Chloroethoxy ) *th*n«
l»i« (2~Chloro«thy 11 ether
Chloroform
t^MMO-M***
l-Cbloro-3-nitrob«nzen«
Chjcoaic »c Id
Chro.iu.
Chrye«n«
Cobalt
CoM»f
Cresol
Cyanide
Cvanuric acid
CAS Mtutoar
108-90-7
510-15-6
75-00-3
112-26-5
111-44-4
47-64-3
§»-«!-?
121-73-3
7738-94-5
7440-47-3
218-01-9
7440-48-4
7440-50-8
13W-77-3
57-12-5
108-80-5
Haxard
Dcwefltic cnv iron-
Car cino- Reproductive/ Mutagen- Acute Chronic Anbul Minfcal
9«nicity Taratogeniclty iclty Toxic it y effect Toxic ity Toxic ity

X


X X
X
X
X
I
XXX X X
X X

X

X XX


-------
Chemical
1 t 3-Dichlor oprop«n«
Dicofol
DUldrin
DlethylphU-l.t.
Dilsobutyl krtoM
^ Di»*thylamino«thyl
_» Mthacrylate
DUwthy Ian i line
Dlaethylnitroaamine
a , 4-DiMthy Iphenol
n-DLoctyl phthalate
1,4-DioxaiM
DlphenylethaiM
Bndrin
Ethanol
Ethanolaalne
CAS Nmb«c
M2-75-6
US- 32-2
§0-57-1
ai-ff-2
, IOS-83-8
2439-35-2
121-69-7
62-75-9
105-67-9
117-B4-0
123-91-1
103-29-7
«-M-i
64-17-5
141-43-5
Haaacd
DcMeatic Environ
Carcino- Reproductive/ Hutagen- Acute Chronic Animal mental
genicifey Teratogeniclty iclty Toxic it y Effect Toxic it y Toxic It*
X
XX
XXX X
X X

•
X X XX

X
X X

X I X X X
X X


-------
                                                                           Hazard
Cheaical
06CP (Dibrooochloropropwi*)
p,p'-DOB
p,p'-DOO
O.p'-OOP
DDT IP*P'J
O.p'-Wr
6N Dlb«nio(a,h) anthracene
r \
v /^ Dicfalorob«nK«n*
1,1-Dichlotoethane
1,2-Dichloro.th.n.
1 , 1-Oichloroethy lene
1 , 2-tcan»-Oichloroethy lene
2,4-DlcoLocophenol
2,4-oichlorophenoxy
CAS timber
94-12-18
72-55-9
«-5«-i
53-19-0
50-29-3
789-02-4
53-70-1
95-50-1
75-34-3
107-04-2
7S-35-4
156-40-5
120-03-2
§4-75-7
Catcino- Reproductive/ Hutagen- Acute Chronic
genicity Teratogenlcity icity foxiclty Effect
X X X
XX X
XX X
XX X
XX X
XX X
X X


X XX
XXX


X X
Doatestic Environ
Aniiaal Mntal
Tox icity foxicitj

X X
X X
X X
X X
X X
•





X

acetic acid
,2-Dichloropcopane
                              18*87-5

-------
Haiard
*»
Chealcal
Ethyl acetate
Bthylbeniene
Bthylene glyool
Bthyl ether
Bthyl hexanediol
*" bia-2-BthylhexyL ph thai ate
Fluor an thene
rluorene
rorsaldehyde
Ueptachlor
Hexachloroboniene
Bexachlorobutadlene
Hexachlorocyclohexane
Hexach loco«t h«n«
Hexachlorophene
Hexane
Doeteatlc Environ
Carclno- Reproductive/ Mutagen- Acute Chronic Anival Mental
CAfl Mu-Jber genlcity Teratogenlclty icity Tonlclty BCCect Toxlclty Toxicit)
141-78-6
100-41-4 I
107-21-1 • I
60-29-7 I
94-96-2
117-01-7 I *
206-44-0
86-73-7
50-00-0 I III
76-44-8 1 I I I X X X
110-74-1 I I III
07-«0-3 1 ill
600-73-1 I I »
S7-71-1 1
70-30-4 X X
110-54-3 X 1

-------
Hazard
Chmical
Ind«no(l,2,3-od) pyren*
Iron
Ivobutyl alcohol
Icopropyl ether
Lead
Lithlua
Mag nee tun
Manganese
Mercury
H*th«orylio «cld
H«th«nol
H«thyl chlotid*
Hethyl*n« chlorld*
Methyl *thyl hetone
Methyl Iflobutyl ketone
CAS HiMkb*r
1*3-39-5
7439-B9-*
76-§3-l
108-20-3
7439-»2-l
7439-93-2
7439-95-4
7439-94-5
7439-97-*
79-41-4
*7-5t-l
M-il-3
7SHI»-a
78-93-1
108-10-1
DoMtakic Environ-
Caret no- Reproductive/ Hutaqen- Acutfi Chronic Aniaal *«ntai
9«nlcity Teratoganictty icity Toiicity Effect Toxiclty Tovictty
I I

I

I III
• •

•
I III II
I
I
III I
I I
X


-------
u
Chealcal
Methyl Mthacrylat*
Methyl parathion
Naphthalene
Nickel
Mitrocelluloee
2-Hitrophenol
4-Nltrophenol
Pentachlorophanol
Phenanthren*
Mienol
Phenyl ether
ftioaphoric acid
Phoaphorua (white}
Picric acid
Polvch lor inated
Hazard
Do»e»tic Environ
Carclno- Reproductive/ Mutagen- Acute Chronic Anisal a«ntal
CM ttuaber 9«nlcity Teratogenictty Iclty Tonic 1 ty Effect Toxic Uy Toitlclt
80-62-6 1 1
298-00-0 11 I 1
•1-20-3 >
7440-02-0 II XI
9004-70-0
•0-7S-S
100-02-7
87-86-5 8 «
OS-01-8 «
108-95-2
101-84-0
7664-30-2
7723-14-0 I « » I I
08-89-1 *
1336-36-1 I M *
           biphenyls

-------
                                                                              Hazard
Cheaical
Polychlorlnated
dlbenvo-p-dioxina
Pyrene
Seleniue)
Silver
Sodiua (aetall
Sodiu* chlorate
Stoddacd eolvent
Sul Curie acid
1,2,4, 5-Tet rachlorobenaene
217 8-T«trachloro-
GAS Hue>ber

m-oo-o
7782-4»-2
7440-22-4
7440-23-5
?77S-«f-f
8052-41-3
7664-»3-»
15~»4-3
1746-01-6
Caret no- Reproductive/
genlclty Teratogenlclty
X X

X






X X
Doematic Bnwiron-
Hutagen- Acute Chronic Anlaal aeiital
Iclty Toxic ity BCCect fovicity Tociclty
XX XX

X XX
X

X



XX XX
  dlbetiso-p-dioxtn



l,lr2,2~T«tr«chloro«tluHie       79-34-5




T« tract) lor o«thylen«            127-18-4



Tetraethyl lead                 78-00-2
X




X
X




X
X




X

-------
chemical
Tetrahydrofuran
Thallium
Titan ilia
Toluene
Toxaphene
Tr ich lorobensene
1,1,1-Tr ich lor oe thane
lv 1 , 2-Tr ich loroe thane
Tr Ichloroethy lene
Tr icbloroC 1 uoroaia thane
CikS Nuafcer
109-99-9
7440-28-0
7440-32-4
LM-M-1
8001-35-2
50-31-7
71-55-6
79-00-5
79-01-*
75-W-4
Hazard
Pnaoatic Bnvirc
Carcino- Reproductive/ Mutagen- Acute Chronic AniiMl atental
genie ity Teratogenicity icity Toxic ity Effect Toviclty Toxic!

X XX

X X
X X X XX

X
X
X X

2,4,5-Tr IchloroohenoKy
  acetic acid

2,4,5-Trichlorophenoxy
  propiooic acid

2,4,5-Trichlorophenol

trla(2« 3-Dlbro«opropyl>
  phosphate
tl-71-l
95-95-4

-------
                                                                              Haiaid


                                                                                                     Doaestic   Environ
                                          Carcino-    Reproductive/   Mutagen-   Acute     Chronic    jyniaal    cental
Chemical                     CAS  Huaber   genicity   Tef«tog«nicity    icity    Toxic ity  effect    foxicity   Tonic it
                              7440-42-2

Vinyl chloride                  75-01-4       z              l

Xylene                        1330-20-7                      I

line                          7440-6S-6

-------
                            APPENDIX 9
                          CAG OMIT RISK

     The Carcinogen Assessment Group  {CAG) of BPA has performed
quantitative risk assessments on numerous chemicals.  These
assessments were performed using data from the best available
studies at the tine the assessment was performed; the data
were fitted to the particular mathematical model considered
moat appropriate.  A "unit risk," defined as the lifetime cancer
risk to humans associated with continuous exposure to a unit
dose of 1 mg/kg/day, was calculated.  The 95th pereentile upper
confidence Unit for unit risk Is given in the following table
as a slope.  This value can be divided into the generally accep-
table lifetime risk of 10"6 to determine the dally dose in
ag/kg/day associated with this risk  level.  It should be stressed
that the data used to generate the unit risk numbers and the
methods of extrapolation are relatively inexact and utilize
conservative assumptions; therefore,  the milt elsk values should
only be considered as at best, order  of magnitude approximations
of the upper limit on potential risk.  This Is reflected in
the last column of the following table, which indicates the
potency oC each chemical«to order of  magnitude on a logarithmic
scale.  On this scale, a chemical with an index of 4-6 is about
one million (10*) times more potent  than a chemical with an
index of zero.
                                                  ciamanc AMOCWtM

-------
RELATIVE CARCINOGENIC POTENCIES AMONG 54 CHEMICALS EVALUATED IY THE CAICINOCEM ASSESSMENT CROUP
                          AS SUSPECT HUMAN CAHCINOGEMS
Grouping
Level baaed on
of evidence* 1A1C Slope1*
Coapounda CAS Number Huauina
Acrylonltrile 107*11-1
Af la toxin 1| I 162-6 SHI
Aldrle 309-00*2
f
Allyl chloride 107-05-1
Areenlc 7440—34—2
•i«lr so-)2-8
•emcee 71-43-2
•enaldene 92-87-S
fterflliuai 7440-41-7
1.3-tutadlena . 106-99-0
CedBliax 7440*43-9
Carbon tetrechloride 56-2)-$
Chlordane 51-74-9
L
L
1

S
t
S
S
L
1
L
1
1
Anlnele criteria (eig/kg/day V1
S
S
L
-
1
S
S
8
8
S
S
S
L
2A
2*
21

1
2t
1
1
2A
21
2A
21
1
0.24(11)
2900
11.4
1.19*10-*
15(10
ll.S
2.9xlO-2(lf)
2)4(11)
2.6
l.Om!0-lW
6.i(tt)
1.30.10-i
1.61
Molecular Potency
weight Index0
53.1 UIO*»
312.) 9»10*5
369.4 4.10*3
76.4 9mlO*1
149.8 2mlO^
2S2.) 3»10*3
78 2x10°
184.2 4*10+*
9 2.10*1
14. 1 5x10°
112.4 7x10*2
153.8 2x10+*
409.8 ?«10+2
Order of
•egnltude
Index)
+1
+6
44
0 .
•3
*3
0
+5
+1
+1
+3
+i
+3
                                                                 (continued on the following peg*}

-------
Level
*••»•••*
^S^S*
CAS Hiakfr •
107-04-2
47-72-1
l.l,2.2-T«trachloroetkue 79-34-5
1,1 ,2-TrlchloroothMO 79^0-5
Chlerofora
CfcraajlMBVI
•Dt
^
1 ,1-ftlcklarMtbylMM
(VierlleeM chlorioe)
MckloroeetluM
(Nttkf !*•* chloride)
DleUrU
2,4-Oleltrocelu*M
I tpichiorobydrie
it
> •le(2-chloroethyl)etiier
i
47-44-3
7440-47-3
SO-29-1
fl^V-i
7J-35-*
75-09-2

40-J7-1
121-14-2
122-44-7
I04-t9-t
111-44-4
um»m»
1
1
1
1
1
S
I
I
1
I

I
1
1
1
1
AoU.1.
S
L
L
L
S
S
8
8
L
L

•
f
§
s
s
Croup lag
iMMMNl M
1ARC
erltorla
2S
1
3
1
21
1
21
21
1
S

21
21
21
21
21
81op«b Mbl*cular
(««Ag/«Uy)-l wight
9. 1m 10-2
0.20
S.71mIO-J
7.10-t
41(W)
0.34
1.49
1.14(1}
4.3*10-* (I)

30.4
0.11
0.77
9.9>10*3
1.14
98. »
234.7
147.9
133.4
119.4
100
354.5
253.1
97
•4.9

3M.9
182
ISO
92. S
143
icoatlouod o
Order of
MgftlttMU
Potency U<»t|o
9x10° *l
3x10° 0
8.10° 4-1
•xlO* *1
4»10*3 44
IxlO4^2 +2
4.10*2 +3
UIO*2 +2
IxMT* -I

ixIO" 44
4.10*1 4-2
1*10*2 +2
9*IO-» 0
J,IO« «


-------
              Grouping
   Level      baaed on
of evidence*    IMC
Compound*
                         CAS fenber KiMM  AnlMle criteria
                                                                Slop«i
                                                                                     Holeoular
                                                                                             Potency
                                                                                                       Order of
                                                                                                       •a§nltud«
                                                                                                                lAdam)
      •ia(cbloroa»tbyl)atbar

      ttbylene dlbcovlde (EOi)

      Itaylane

      Heatacblor

      Ueiacblorobai
                         S41-W-1
£
 *
                          75-21-f

                          74-44-8

                          lit-74-1

                          8?~t8-l
He aachlorocyclohevan*
  technical §r«d«

  beta laoewr
      HeucklorodibeuodtoUa

      Hlckal                    7440-O2-O
 S

 1

 L

 1

 1

 1




 1
 I
 I

 I

 L
 Dlhutylnltroacaln*
                                   ss-ia-s
                                  924-lfr-l
                                               S

                                               S

                                               S

                                               s

                                               s

                                               L
S
L
L

8

8
                                               s
                                               s
                                               s
                                               8
                                               S
        I

        a

        u

        21

        28
28
1
28

28

24
                 2t
                 21
                 21
                 21
           9100CE1

           41
           1.17

           1.47
4.7S
11.12
1.84
1.11
                                                                 1.
                   2S.9(Mt by
                   41 S{a4it by
                   S.41
                   2.11
                   12.9
US

187.9

 44.1

171.1

284.4

261


290.9
290.9
290.9
290.9

391

 58.7
                             74.1
                            102.1
                            IS8.2
                            100.2
                            117.1
                           8BIO+*

                           2*10**
                                                                                            1,10*1
+1

41


41


41

46

42


4J

41

44
                                                                             (continuedon Che following page)

-------
                  level
               af evidence*
CIS Nuaher   Muaaae  aalaala
                                                          Group Ing
                                                          baaed aa
                                                            1AIC
                                                          crltarla
                                       Orair af
ilapa
                                                                                      Nalacular    Foteacy
                                                                                                              laa..)
M-»t t roea-tt-aathy luraa
V-vltroea^diphaaylaalaa
Kla
Vhaaala
2.4,4-Trlchlarapheaal
Tetrachloradlbeaxo- ,
p-dloila (TCDO)
fatrachlaraathylaaa
lamaah^a
Trlchlaraatbylaaa
aa4-t3-i
•4*30-4
1334-34-)

M-44-2

I744-OI-4
127-1B-4
•001-31-2
79-01-4
I
1
1

1

1
1
I
I
S
S
s

s

s
L
1
L/S
21 302.4
21 4.*2KUT>
21 4.34

21 I.MilO-I

21 I.MilO+3
3 S.I.IO'*
21 1.13
3/21 I.UIOT*
103. 1
III
324

Itl.4

322
14S.I
414
131.4
3«IO**
1x10^
ImlO*^

4mlO°

»«!«*'
••10°
SxlO
Iftlfr**
44
0
43

+1

«§
«1
+J
0
flayl chlarlda
                                                             1
                  42. S
                                                                          ImlO0
•S - S«If Iclaat andaacai L - LLaitad amaaacas  I *  laada^uaca awaaaca.
•aataal alaaaa ara *5X upaar»bouad alapaa  baeed  aa tha llaaarUed aultlataga aodel.  They ara calculatad based aa
 aalaal aral atudlaa, aicapt far thoae  tadlcatad by  1  laalaa 1  lahalatlaa)c H (hiouia aceaaatlaaal expoewra), aai M
 (buaaa drlahlag water axpoaMra).  HuMaa alapaa  ara  palat aatlaetaa  beeed aa tha llaaar aaatbraahald aaltl»  Mat all
 af tha carclaagaalc pataaclaa preeeated la thla tahla rapraaaat  tha aaaa dagraa af cartalaty.  411 ara aubject ta
 chaaga aa aati avlaaaca bacaaaa available.  Tha  alapa  vatwa la aa upper bauad la tha saaaa that tha true value (which
 ta wotaowa) la aat likely ta aaceed tha upper bound ead aay ba mieh lower, with a lower bound appraachlag lera.
 Thue, tha asa af tha alapa aatlaata la rl>k avaluatlaaa require* aa appraclatlaa far tha lapllcettaa af tha uapar
 bouad eaacapt aa well a* tha "weight ef evidence" far tha  likelihood that tha avbataaca la a buaaa carclaagaa.
'The pataacy ladea la a rouaded-aff alapa  la (•»I/kg/day)~' ead  la  calculated by Multiplying tha alapaa la
           )"» by the •oleoular weight  af  the ceapauad.
                                                               SOU(C«I
U.S. Cnvlroiw«nt*I Protect ion tqency  lUtttAI.   It!
Health *»•••••«* OociaMut for Chlorolor*.  Offlo*
nf Henltk *n4 fnui rnnivntal  Kmtmrnmrnmnt . M**hlnnta«

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-------