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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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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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
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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
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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««
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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
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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
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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
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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
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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
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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-«
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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
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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
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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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best available copy.
-------
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
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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
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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
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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
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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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Preceding page blank
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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
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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
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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
-------
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
-------
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
-------
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
-------
-------
&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
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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
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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»«
-------
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
-------
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
-------
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
-------
-------
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
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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%
-------
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
\
-------
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
-------
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
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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
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October 1985
o*m«nt Aeeeeietee
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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
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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
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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
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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
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October 1915
Preceding page blank
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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_
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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
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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
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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
-------
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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
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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
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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/
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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
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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
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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
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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
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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
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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
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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
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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
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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
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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
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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
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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
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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
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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
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(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
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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
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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
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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
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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
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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
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_ 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
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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
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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
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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
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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*—
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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
-------
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
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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
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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
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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
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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
-------
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
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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
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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
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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
-------
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
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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
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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
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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
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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
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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
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October 1985
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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
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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
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
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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
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October 1985
Preceding page Wank
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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
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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
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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
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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
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October 1985
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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
-------
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
-------
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
-------
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
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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
-------
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
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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
-------
-------
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
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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
Preceding page blank
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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
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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
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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
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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
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October 1985
iacaa
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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
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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
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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
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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°
-------
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
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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
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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
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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
-------
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
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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
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=l-m*nc
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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
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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
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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
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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
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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
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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
-------
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
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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
-------
-------
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
-------
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
-------
-------
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
-------
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
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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
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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
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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
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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
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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
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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
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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
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October 1985
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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
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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
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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
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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
-------
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
-------
-------
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^
-------
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
-------
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>
-------
-------
,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
-------
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
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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
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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
-------
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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
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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
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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
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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
-------
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
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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
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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
-------
....... _, 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 "* ' '
-------
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
-------
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
-------
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
>'
-------
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
-------
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
-------
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
-------
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
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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
-------
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
-------
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
-------
-------
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
-------
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
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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\
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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*
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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
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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
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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
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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
Preceding page blank
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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
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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 <
-------
±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
-------
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
-------
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
-------
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
-------
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
-------
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
Ǥ
«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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