EPA-540/1-86-034
&EPA
Office of Emergency and
Remedial Response
Washington DC 20460
Off'ce of Research and Development
Office of Health and Environmental
Assessment
Environmental Criteria and
Assessment Office
Cincinnati OH 45268
Superfund
HEALTH EFFECTS ASSESSMENT
FOR 2,4,5-TRICHLOROPHENOL
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EPA/540/1-86-034
September 1984
HEALTH EFFECTS ASSESSMENT
FOR 2.4,5-TRICHLOROPHENOL
U.S. Environmental Protection Agency
Office of Research and Development
Office of Health and Environmental Assessment
Environmental Criteria and Assessment Office
Cincinnati, OH 45268
U.S. Environmental Protection Agency
Office of Emergency and Remedial Response
Office of Solid Waste and Emergency Response
Washington, DC 20460
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DISCLAIMER
This report has been funded wholly or In part by the United States
Environmental Protection Agency under Contract No. 68-03-3112 to Syracuse
Research Corporation. It has been subject to the Agency's peer and adminis-
trative review, and H has been approved for publication as an EPA document.
Mention of trade names or commercial products does not constitute endorse-
ment or recommendation for use.
11
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PREFACE
This report summarizes and evaluates Information relevant to a prelimi-
nary Interim assessment of adverse health effects associated with 2,4,5-tr1-
chlorophenol. All estimates of acceptable Intakes and carcinogenic potency
presented In this document should be considered as preliminary and reflect
limited resources allocated to this project. Pertinent toxlcologlc and
environmental data were located through on-line literature searches of the
Chemical Abstracts, TOXLINE, CANCERLINE and the CHEMFATE/DATALOG data
bases. The basic literature searched supporting this document 1s current up
to September, 1984. Secondary sources of Information have also been relied
upon in the preparation of this report and represent large-scale health
assessment efforts that entail extensive peer and Agency review. The fol-
lowing Office of Health and Environmental Assessment (OHEA) source has been
extensively utilized:
U.S. EPA. 1980a. Ambient Water Quality Criteria for Chlorinated
Phenols. Environmental Criteria and Assessment Office, dndnati,
OH. EPA 440/5-80-032. NTIS PB 81-117434.
The Intent 1n these assessments Is to suggest acceptable exposure levels
whenever sufficient data were available. Values were not derived or larger
uncertainty factors were employed when the variable data were limited 1n
scope tending to generate conservative (I.e., protective) estimates. Never-
theless, the Interim values presented reflect the relative degree of hazard
associated with exposure or risk to the chemical(s) addressed.
Whenever possible, two categories of values have been estimated for sys-
temic toxicants (toxicants for which cancer is not the endpolnt of concern).
The first, the AIS or acceptable intake subchronic, is an estimate of an
exposure level that would not be expected to cause adverse effects when
exposure occurs during a limited time Interval (i.e., for an interval that
does not constitute a significant portion of the lifespan). This type of
exposure estimate has not been extensively used or rigorously defined, as
previous risk assessment efforts have been primarily directed towards
exposures from toxicants in ambient air or water where lifetime exposure is
assumed. Animal data used for AIS estimates generally include exposures
with durations of 30-90 days. Subchronic human data are rarely available.
Reported exposures are usually from chronic occupational exposure situations
or from reports of acute accidental exposure.
The AIC, acceptable intake chronic, 1s similar 1n concept to the ADI
(acceptable dally intake). It is an estimate of an exposure level that
would not be expected to cause adverse effects when exposure occurs for a
significant portion of the Hfespan [see U.S. EPA (1980b) for a discussion
of this concept]. The AIC 1s route specific and estimates acceptable expo-
sure for a given route with the implicit assumption that exposure by other
routes is Insignificant.
111
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Composite scores (CSs) for noncarclnogens have also been calculated
where data permitted. These values are used for ranking reportable quanti-
ties; the methodology for their development 1s explained 1n U.S. EPA (1983a).
For compounds for which there 1s sufficient evidence of cardnogenlcHy,
AIS and AIC values are not derived. For a discussion of risk assessment
methodology for carcinogens refer to U.S. EPA (1980b). Since cancer 1s a
process that Is not characterized by a threshold, any exposure contributes
an Increment of risk. Consequently, derivation of AIS and AIC values would
be Inappropriate. For carcinogens, q-|*s have been computed based on oral
and Inhalation data 1f available.
1v
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ABSTRACT
In order to place the risk assessment evaluation 1n proper context,
refer to the preface of this document. The preface outlines limitations
applicable to all documents of this series as well as the appropriate Inter-
pretation and use of the quantitative estimates presented.
A number of subchronlc oral studies have been conducted by the same
group of Investigators. The longest treatment period was 98 days and
Involved dietary administration of 2,4,5-trlchlorophenol to rats. Based on
this study an AIS of 70 mg/day and an AIC of 7.0 mg/day were estimated.
These estimates, especially the AIC, should be reviewed when additional data
are available. A CS of 13 was calculated based on liver and kidney degener-
ation observed In rats fed a diet containing 3000 ppm 1n the 98-day dietary
study by McColllster et al. (1961).
Pertinent data regarding the potential toxlcologlcal effects of Inhaled
2,4,5-trlchlorophenol could not be located 1n the available literature.
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ACKNOWLEDGEMENTS
The Initial draft of this report was prepared by Syracuse Research
Corporation under Contract No. 68-03-3112 for EPA's Environmental Criteria
and Assessment Office, Cincinnati, OH. Dr. Christopher DeRosa and Karen
Blackburn were the Technical Project Monitors and Helen Ball was^the Project
Officer. The final documents In this series were prepared for the Office of
Emergency and Remedial Response, Washington, DC.
Scientists from the following U.S. EPA offices provided review comments
for this document series:
Environmental Criteria and Assessment Office, Cincinnati, OH
Carcinogen Assessment Group
Office of A1r Quality Planning and Standards
Office of Solid Waste
Office of Toxic Substances
Office of Drinking Water
Editorial review for the document series was provided by:
Judith Olsen and Erma Durden
Environmental Criteria and Assessment Office
Cincinnati, OH
Technical support services for the document series was provided by:
Bette Zwayer, Pat Daunt, Karen Mann and Jacky Bohanon
Environmental Criteria and Assessment Office
Cincinnati, OH
v1
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TABLE OF CONTENTS
1.
2.
3.
4.
5.
ENVIRONMENTAL CHEMISTRY AND FATE
ABSORPTION FACTORS IN HUMANS AND EXPERIMENTAL ANIMALS . . .
2.1.
2.2.
ORAL
INHALATION
TOXICITY IN HUMANS AND EXPERIMENTAL ANIMALS
3.1.
3.2.
3.3.
3.4.
SUBCHRONIC
3.1.1. Oral
3.1.2. Inhalation
CHRONIC
3.2.1. Oral
3.2.2. Inhalation
TERATOGENICITY AND OTHER REPRODUCTIVE EFFECTS. . . .
3.3.1. Oral
3.3.2. Inhalation
TOXICANT INTERACTIONS
CARCINOGENICITY
4.1.
4.2.
4.3.
4.4.
HUMAN DATA
4.1.1. Oral
4.1.2. Inhalation
BIOASSAYS
4.2.1. Oral
4.2.2. Inhalation
OTHER RELEVANT DATA
WEIGHT OF EVIDENCE
REGULATORY STANDARDS AND CRITERIA
Page
1
3
. . . 3
3
4
4
. . . 4
. . . 5
, , , 5
. . . 5
5
5
. . . 5
. . . 5
5
6
6
. . . 6
6
. . . 6
. . . 6
6
. . . 6
, , , 6
. . . 8
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TABLE OF CONTENTS (cont.)
Page
6. RISK ASSESSMENT 9
6.1. ACCEPTABLE INTAKE SUBCHRONIC (AIS) 9
6.1.1. Oral 9
6.1.2. Inhalation 9
6.2. ACCEPTABLE INTAKE CHRONIC (AIC).
6.2.1. Oral 9
6.2.2. Inhalation 10
6.3. CARCINOGENIC POTENCY (q-\*) 10
8. REFERENCES 11
APPENDIX: Summary Table for 2,4,5-TMchlorophenol 14
V111
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LIST OF ABBREVIATIONS
ADI Acceptable dally Intake
AIC Acceptable Intake chronic
AIS Acceptable Intake subchronlc
BCF Bloconcentratlon factor
bw Body weight
CAS Chemical Abstract Service
CS Composite score
DMBA D1methybenz[a]anthracene
LOAEL Lowest-observed-adverse-effect level
MED Minimum effective dose
NOEL No-observed-effect level
ppm Parts per million
RVd Pose-rating value
RVe Effect-rating value
UF Uncertainty factor
1x
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1. ENVIRONMENTAL CHEMISTRY AND FATE
The relevant physical and chemical properties and environmental fate of
2,4,5-trlchlorophenol (CAS No. 95-95-4) are given 1n Table 1-1.
The half-life values for 2,4,5-trlchlorophenol 1n air and aquatic media
were not located In the available literature; however, based on the specu-
lated fate of Its Isomer (see accompanying report on 2,4,6-tMchlorophenol),
photodecomposHlon 1n the atmosphere 1s expected to be the dominant fate of
this compound. Similarly, photodecomposHlon 1s expected to play a signifi-
cant role 1n determining the fate of this chemical 1n aquatic media since
this compound may be resistant to microblal degradation (U.S. EPA, 1980a).
In the absence of quantitative data pertaining to the rate of photodecompo-
sHlon, H 1s not possible to predict the half-lives of this chemical 1n air
and aquatic media.
The octanol/water partition coefficient value given 1n Table 1-1 Indi-
cates that this compound may be significantly sorbed to soils with high
organic carbon content. In sandy soils, 2,4,5-trlchlorophenol may have
significant mobility. The b1odegradab1!1ty and aqueous solubility of this
compound are such that leaching of this compound, especially from sandy soil
to groundwater, 1s possible.
-1-
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TABLE 1-1
Selected Physical and Chemical Properties and
Half-Lives for 2,4,5-TMchlorophenol
Properties
Values
References
Chemical class:
Vapor pressure:
Water solubility:
Log octanol/water
partlon coefficient;
BCF:
Residence time
1n soil:
halogenated phenol
1 mm at 72°C
1190 mg/kg at 25°C
3.72
290
110
>72 days for complete
disappearance
NA
Weast, 1980
Verschueren, 1983
U.S. EPA, 1980a
VeHh et al., 1979
U.S. EPA, 1980a
Verschueren, 1983
NA = Not applicable
-2-
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2. ABSORPTION FACTORS IN HUMANS AND EXPERIMENTAL ANIMALS
2.1. ORAL
No quantitative studies of absorption following oral exposure of humans
or animals to 2,4,5-tMchlorophenol could be located 1n the available liter-
ature. Dougherty and Plotrowska (1976) suggested that chlorophenols as a
class tend to be eliminated rapidly 1n the urine; therefore, urinary concen-
trations reflect exposure. Quantitative analyses were not performed 1n this
study.
Kutz et al. (1978) analyzed 418 samples of urine collected from the
general population as part of a health and nutritional survey. Residues of
2,4,5-tMchlorophenol were found In 1.7% of the samples. The average
concentration found was <5 yg/l and the maximum was 32.4 yg/S,.
2.2. INHALATION
Pertinent data regarding the absorption of 2,4,5-tMchlorophenol fol-
lowing Inhalation exposure could, not be located 1n the available literature.
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3. TOXICITY IN HUMANS AND EXPERIMENTAL ANIMALS
3.1. SUBCHRONIC
3.1.1. Oral. McCoTMster et al. (1961) conducted a variety of toxIcHy
studies on 2,4,5-trichlorophenol 1n rats and rabbits. Groups of rabbits
(number and sex unspecified) were given 20 dally oral (gavage) doses of 1,
10, 100 or 500 mg 2,4,5-trlchlorophenol/kg bw over a 28-day period. "Very
slight kidney changes" and "very slight liver and kidney changes" were found
1n one rabbit each from the 100 mg/kg and 500 mg/kg groups, respectively.
No effects were found 1n five rabbits given 1 or 10 mg/kg dally.
Concurrently, McColllster et al. (1961) administered 18 daily doses of
0, 30, 100, 300 or 1000 mg 2,4,5-trichlorophenol/kg bw in olive oil to
groups of five male rats over a 24-day period. Rats treated with 1000 mg/kg
bw experienced a small amount of weight loss (-10 g; initial body weight
-270 g) during the first 10 days, but recovered quickly and were gaining
weight normally by day 14. Upon necropsy, high dose rats were found to have
slight kidney enlargement when compared to control rats. No other effects
of treatment were found; in this study, 300 mg 2,4,5-trlchlorophenol/kg bw
was a NOEL in rats.
McColllster et al. (1961) also maintained groups of 10 male and 10
female rats on diets containing 100, 300, 1000, 3000 or 10,000 ppm 2,4,5-
trichlorophenol for 98 days. Mild diuresis and slight degenerative changes
in the liver and kidneys were noted in rats of both sexes in the 3000 and
10,000 ppm groups. Reported pathological lesions 1n the liver consisted of
mild centrilobular degenerative changes characterized by cloudy swelling and
occasional areas of focal necrosis. Slight proliferation of the bile ducts
and early portal cirrhosis were also observed. The kidneys showed moderate
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changes 1n the epithelium of the convoluted tubules and "early prolifera-
tion" of the Interstitial tissue. These changes were considered to be mild
and reversible. Judging from behavior, mortality, food consumption, growth,
terminal hematology, body and organ weights and gross and microscopic
pathology, 1000 ppm was considered to be a NOEL.
No studies of subchronlc oral exposure of humans to 2,4,5-tMchloro-
phenol could be located 1n the available literature.
3.1.2. Inhalation. No reports of toxldty In humans or animals associ-
ated with Inhalation exposure to 2,4,5-tMchlorophenol could be located 1n
the available literature.
3.2. CHRONIC
3.2.1. Oral. No studies of toxldty associated with chronic oral expo-
sure to 2,4,5-tMchlorophenol in humans or animals could be located 1n the
available literature.
3.2.2. Inhalation. No studies of toxldty associated with chronic Inha-
lation exposure to 2,4,5-tMchlorophenol could be located 1n the available
literature.
3.3. TERATOGENICITY AND OTHER REPRODUCTIVE EFFECTS
3.3.1. Oral. No reports of teratogenldty In humans or animals asso-
ciated with oral exposure to 2,4,5-tMchlorophenol could be located 1n the
available literature.
3.3.2. Inhalation. No reports of teratogenldty In humans or animals
associated with Inhalation exposure to 2,4,5-tMchlorophenol could be
located 1n the available literature.
3.4. TOXICANT INTERACTIONS
No studies of the Interactions of 2,4,5-trlchlorophenol with other xeno-
blotlcs could be located 1n the available literature.
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4. CARCINOGENICITY
4.1. HUMAN DATA
4.1.1. Oral. No reports of carc1nogen1c1ty 1n humans associated with
oral exposure to 2,4,5-trlchlorophenol could be located In the available
literature.
4.1.2. Inhalation. No reports of cardnogenlcHy 1n humans associated
with Inhalation exposure to 2,4,5-trlchlorophenol could be located 1n the
available literature.
4.2. BIOASSAYS
4.2.1. Oral. No studies of the cardnogenlcHy of orally administered
2,4,5-trlchlorophenol could be located 1n the available literature.
4.2.2. Inhalation. No studies of the cardnogenlcHy of 2,4,5-trlchloro-
phenol administered by Inhalation could be located 1n the available litera-
ture.
4.3. OTHER RELEVANT DATA
Rasanen et al. (1977) tested 2,4,5-trlchlorophenol for mutagenldty In
the Ames assay using Salmonella typhlmuMum strains TA98, TA100, TA1535 and
TA1537. Negative results were reported both 1n the presence and absence of
rat hepatic S9 fraction. Details of protocol were not available.
Repeated spraying of the flower buds of vetch (V1c1a faba) with an
aqueous solution of 2,4,5-trlchlorophenol Increased the frequency of abnor-
malities In pollen mother cells, Including stickiness and chromosomal lag-
ging during cell division and an Increased Incidence In fragmented chromo-
somes (Amer and All, 1974).
4.4. WEIGHT OF EVIDENCE
No reports of cancer 1n humans associated with 2,4,5-trlchlorophenol and
no bloassays of the cardnogenlcHy of 2,4,5-trlchlorophenol In laboratory
animals could be located 1n the available literature.
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Boutwell and Bosch (1959) treated 20 female Sutter mice with a single
application of 75 yg DMBA on the dorsal skin as a tumor Initiator.
Approximately 1 drop of commercial grade 2,4,5-trlchlorophenol (-25 yl)
1n acetone was applied twice weekly for 16 weeks as a tumor promoter. Skin
paplllomas were observed in 8/19 surviving mice. No skin tumors were found
1n 18 surviving controls treated with acetone alone, and 1 tumor was found
1n 21 surviving male mice (strain unspecified) treated with 75 yg DMBA
alone. No mice were treated with 2,4,5-trlchlorophenol alone.
Applying the criteria proposed by the Carcinogen Assessment Group of the
U.S. EPA for evaluating the overall weight of evidence of carcinogenidty
for humans (Federal Register, 1984), 2,4,5-trlchlorophenol is most appropri-
ately classified a Group D - Not Classified chemical.
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5. REGULATORY STANDARDS AND CRITERIA
No current standards or criteria for 2,4,5-trlchlorophenol 1n air were
located 1n the available literature.
The U.S. EPA (1980a) calculated an interim ADI of 7 mg 2,4,5-trichloro-
phenol/day for a 70 kg human, based on the NOEL of 1000 ppm from the 98-day
oral study in rats by McCollister et al. (1961), assuming that rats eat food
equivalent to 10% of their body weight/day and applying a UF of 1000.
Assuming that humans drink 2 8. of water/day and eat 6.5 g of fish, which
bioaccumulate 2,4,5-trichlorophenol by a factor of 110 (U.S. EPA, 1980a), an
ambient water quality criterion of 2.6 mg/s, was determined by the U.S. EPA
(1980a). If human exposure is assumed to be from the consumption of fish
and shellfish alone, an ambient water quality criterion of 9.8 mg/s, has
been determined to be protective. On the basis of organoleptic effects, a
criterion of 1.0 yg/5- has been suggested.
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6. RISK ASSESSMENT
6.1. ACCEPTABLE INTAKE SUBCHRONIC (AIS)
6.1.1. Oral. McColHster et al. (1961) exposed rats of each sex to diets
containing 100, 300, 1000, 3000 or 10,000 ppm 2,4,5-tMchlorophenol for 98
days. M1ld pathological changes 1n the kidneys and liver were observed 1n
rats of both sexes exposed to diets containing 3000 or 10,000 ppm 2,4,5-trl-
chlorophenol. No effects were observed 1n rats exposed to 1000 ppm, and
this level was judged to be a NOEL. Assuming that young, growing rats
consume food equivalent to 10% of their body weight/day, this diet resulted
1n an animal Intake of 100 mg/kg/day. An AIS can be calculated by multiply-
ing the animal dose, 100 mg/kg/day, by 70 kg (the average weight of a man)
and dividing by an UF of 100 (a factor of 10 to account for Interspedes
extrapolation and a factor of 10 to protect unusually sensitive groups 1n
the population). An AIS of 70 mg/day 1s calculated.
6.1.2. Inhalation. No data concerning subchronlc Inhalation exposure of
humans or animals to 2,4,5-tMchlorophenol have been located 1n the avail-
able literature; hence, no AIS for subchronlc Inhalation exposure can be
calculated.
6.2. ACCEPTABLE INTAKE CHRONIC (AIC)
6.2.1. Oral. Data from the study by McColHster et al. (1961), from
which an AIS of 70 mg/day 1n humans was calculated, can be used to derive an
AIC for oral exposure, since no studies of truly chronic oral exposure were
found. Application of an additional UF of 10 to convert from a subchronlc
NOEL to a chronic NOEL results in an AIC for oral exposure of 7.0 mg 2,4,5-
trlchlorophenol/day.
U.S. EPA (1983b) computed a CS for the effects of mild diuresis and
slight degenerative changes 1n the liver and kidneys observed by McColHster
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et al. (1961) 1n rats fed diets containing 3000 ppm 2,4,5-tMchlorophenol.
Assuming rats eat food equivalent to 5% of their body weight/day, the effec-
tive animal dose 1s 150 mg/kg/day. The equivalent human MED, 179.6 mg/day,
1s calculated by multiplying the animal dose by the cube root of the ratio
of the body weight of rats (assumed: 0.35 kg) to that of humans (assumed: 70
kg), applying an UF of 10 to convert from subchronlc to chronic exposure,
and multiplying the result by 70 to express the dose as mg/day for a 70 kg
human. This MED corresponds to an RVd of 2.1. The effects observed, mild
diuresis and degenerative changes In the Hver and kidney, warrant an RV
of 6. A CS of 13, the product of RV. and RV , results.
6.2.2. Inhalation. No reports of toxldty 1n humans and animals asso-
ciated with chronic Inhalation exposure to 2,4,5-tMchlorophenol could be
located In the available literature; hence, no AIC for chronic Inhalation
exposure can be calculated.
6.3. CARCINOGENIC POTENCY (q^)
No reports of cardnogenldty 1n humans or animals exposed to 2,4,5-tr1-
chlorophenol by either the oral or the Inhalation route could be located 1n
the available literature. No carcinogenic potency estimate can be made for
either oral or Inhalation exposure to 2,4,5-trlchlorophenol.
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8. REFERENCES
Amer, S.M. and E.M. All. 1974. Cytologlc effects of pesticides. V.
Effects of some herbicides on Specla faba. Cytologla. 33: 633. (Cited In
NIOSH, 1981)
Boutwell, R.K. and O.K. Bosch. 1959. The tumor-promoting action of phenol
and related compounds for mouse skin. Cancer Res. 19: 413-424. (Cited In
U.S. EPA, 1980a)
Dougherty, R.C. and K. Plotrowska. 1976. Screening by negative chemical
1on1zat1on mass spectrometry for environmental contamination with toxic
residues: Application to human urines. Proc. Natl. Acad. Sc1., USA. 73:
1777-1781. (Cited In U.S. EPA, 1980a)
Federal Register. 1984. Environmental Protection Agency. Proposed guide-
lines for carcinogenic risk assessment. 49 FR 46294-46299.
Kutz, F.W., R.S. Murphy and S.C. Strassman. 1978. Survey of Pesticide
Residues and Their Metabolites 1n Urine from the General Population. Jji:
Pentochlorophenol: Chemistry, Pharmacology and Environmental Toxicology,
K.R. Rao, Ed., Plenum Press, NY. p. 363-369. (Cited In U.S. EPA, 1980a)
McColHster, D.D., D.T. Lockwood and V.K. Rowe. 1961. Tox1colog1c Informa-
tion on 2,4,5-tMchlorophenol. Toxlcol. Appl. Pharmacol. 3: 63-70. (Cited
In U.S. EPA, 1980a)
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NIOSH (National Institute for Occupational Safety and Health). 1981.
Information Profiles on Potential Occupational Hazards. Chlorophenols.
Second Draft. Prepared by Syracuse Research Corporation under Contract No.
21-79-0030 for NIOSH, Rockville, MD.
Rasanen, L., M.I. Hattula and A.U. ArstHa. 1977. The mutagenlclty of MCPA
and Its soil metabolites, chlorinated phenols, catechols and some widely
used s!1m1c1des in Finland. Bull. Environ. Contam. Toxlcol. 18: 565-571.
(Cited In U.S. EPA, 1980a)
U.S. EPA. 1980a. Ambient Water Quality Criteria for Chlorinated Phenols.
Environmental Criteria and Assessment Office, Cincinnati, OH. EPA
440/5-80-032. NTIS PB 81-117434.
U.S. EPA. 1980b. Guidelines and Methodology Used in the. Preparation of
Health Effects Assessment Chapters of the Consent Decree Water Quality
Criteria. Federal Register. 45:79347-79357.
U.S. EPA. 1983a. Methodology and Guidelines for Reportable Quantity Deter-
minations Based on Chronic Toxicity Data. Prepared by the Environmental
Criteria and Assessment Office, Cincinnati, OH, OHEA for the Office of Solid
Waste and Emergency Response, Washington, DC.
U.S. EPA. 1983b. Reportable Quantity for 2,4,5-Trichlorophenol. Prepared
by the Environmental Criteria and Assessment Office, Cincinnati, OH, OHEA
for the Office of Solid Waste and Emergency Response, Washington, DC.
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Velth, G.D., D.L. Defoe and B.V. Bergstedt. 1979. Measuring and estimating
the bloconcentratlon factor of chemicals In fish. J. F1sh Res. Board Can.
36: 1040-1048.
Verschueren, K. 1983. Handbook of Environmental Data on Organic Chemistry,
2nd ed. Van Nostrand Relnhold Co., NY. p. 1310.
Weast, R.C., Ed. 1980. CRC Handbook of Chemistry and Physics. CRC Press,
Inc., Boca Raton, FL. p. D207.
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APPENDIX
Summary Table for 2,4,5-Trlchlorophenol
Inhalation
AIS
AIC
Oral
AIS
AIC
Maximum
composite
score
Experimental Acceptable Intake
Species Dose/Exposure Effect (AIS or AIC)
ND
NO
rat 1000 ppm diet none 70 mg/day
(100 mg/kg bw/day)a
rat 1000 ppm diet none 7.0 mg/day
(100 mg/kg bw/day)a
rat 3000 ppm diet (150 mild diuresis, 13
mg/kg bw/day)'3 liver and kidney
(RVd = 2.1)c degeneration
(RVe = 6)
Reference
McColllster
et al., 1961
McColllster
et al., 1961
McColllster
et al., 1961;
U.S. EPA, 1983b
aFood factor of 10% bw assumed for young growing rats
bpood factor of 554 bw was assumed for rats
CUF of 10 was applied to convert from subchronlc to chronic exposures
ND -- Not derived
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