August, 1983
PROPHAM
Health Advisory
Office of Drinking Water
U.S. Environmental Protection Agency
I. INTRODUCTION
The Health Advisory (HA) Program, sponsored by the Office of Drinking
Water (ODW), provides information on the health effects, analytical method-
ology and treatment technology that would be useful in dealing with the
contamination of drinking water. Health Advisories describe nonregulatory
concentrations of drinking water contaminants at which adverse health effects
would not be anticipated to occur over specific exposure durations. Health .
Advisories contain a margin of safety to protect sensitive members of the
population.
Health Advisories serve as informal technical guidance to assist Federal,
State and local officials responsible for protecting public health when
emergency spills or contamination situations occur. They are not to be
construed as legally enforceable Federal standards. The HAs are subject to
change as new information becomes available.
Health Advisories are developed for one-day, ten-day, longer-term
(approximately 7 years, or 10% of an individual's lifetime) and lifetime
exposures based on data describing noncarcinogenic end points of toxicity*
For those substances that are known or probable human carcinogens, according
to the Agency classification scheme (Group A or B), Lifetime HAs are not
recommended. The chemical concentration values for Group A or B carcinogens
are correlated with carcinogenic risk estimates by employing a cancer potency
(unit risk) value together with assumptions for lifetime exposure dnd the
consumption of drinking water. The cancer unit risk is usually derived from
the linear multistage model with 95% upper confidence limits. This provides
a low-dose estimate of cancer risk to humans that is considered unlikely to
pose a carcinogenic risk in excess of the stated values. Excess cancer risk
estimates may also be calculated using the one-toit, Weibull, logit or probit
models. There is no current understanding of the biological mechanisms
involved in cancer to suggest that any one of these models is able to predict
risk more accurately than another. Becaus^ each model is based on differing
assumptions, the estimates that are derived can differ by several orders of
magnitude.

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Pre. am
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GENERAL INFORMATION AND PROPERTIES
CAS No. 122-42-9
Structural Formula
o
N-C-0-CH(CH3)2
I
H
Phenyl 1 -rnethylethyl carbamate; isopropyl-N-phenylcarbamate;
Isoproopyl carbanilate.
Synonyms
* IPC, IFC, Ban-Hoe, Beet-Kleen, Chem-Hoe, Premalox, Triherbide-IPC,
Tuberite (Meister, 1988).
Uses
• Pre- and postemergence herbicide for control of weeds in alfalfa,
clover, flax, lettuce, safflower, spinach, sugarbeets, lentils and
peas -and on fallow land. Prevents cell division. Acts on meristematic
tissue (Meister, 1988).
Properties (Meister, 1988; Cohen, 1984? CHEMLAB, 1985; TDB, 1985)
Chemical formula
Molecular Weight
Physical State (25®C)
Boiling Point (at 25 mm Hg)
Melting Point
Density
Vapor Pressure (25°C)
Specific Gravity (20°C/20#C)
Water Solubility (25»C)
Log Octanol/Water Partition
Coefficient
Taate Threshold
Odor Threshold
Conversion Factor
c10h13°2n
1	79.21
White crystals
87°C
1.0 9 g/mL (20°C)
(sublimes slowly at 2 5°C)
1.09
2	50 mg/L
1.22 (calculated)
Occurrence
° Propham has fc sen found in 1 of 392 surface water samples analyzed
and was undetectable in 583 ground water samples (STORET, 1988).
Samples were collected at 131 surface water locations and 572 ground
water locations, and propham was found in Texas. The 85th percentile
of the sample and the maximum concentration found in surface water
was 2 ug/L. This information is provided to give a general impression
of the occurrence of this chemical in ground and surface waters as
reported in the STORET database. The individual data points retrieved

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Propham
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^ugust, 1983
were used as they came from STORET and have not been confirmed as to
their validity. STORET data is often not valid when individual
numbers are used out of the context of the entire sampling regime, as
they are here. Therefore, this information can only be used to form
an impression of the intensity and location of sampling for a particular
chemical.
Environmental Fate
0 Ring-labeled 14c-propham (purity unspecified), at 4 ppm in unbuffered
distilled water declined to 2.4 ppm during 14 days of irradiation
with a Pyrex-filtered light (uncharacterized) at 2 5°C (Gusik, 1976).
Degradation products included isopropyl 4-hydroxycarbanilate (3.5% of
applied propham), isopropyl 4-aminobenzoate (approximately 0.1%),
1-hydroxy-2-propylcarbanilate (approximately 0.1%), and polymeric
materials (10 to 12%). No degradation occurred in the dark control
during the same period.
° Under aerobic conditions, ring-labeled 14c-propham (test substance
uncharacterized), at 2 ppm, degraded with a half-life of 2 to 7 days in
silt loam soil, (Hardies, 1979; Hardies and Studer, 1979a), 4 to 7 days
in loam soil (Hardies and Studer, 1979b), and 7 to 14 days in sandy
loam soil (Hardies and Studer, 1979c) when incubated in the dark at
approximately 2 5°C and 60% of water holding capacity.
° Under anaerobic conditions, ring-labeled 14c-propham (test substance
uncharacterized) declined from 8.5 to <5% of the applied radioactivity
during 60 days of incubation in silt loam soil in the dark at approxi-
mately 2 5°C and 60% of water holding capacity (Hardies 1979; Hardies
and Studer, 1979a). Under anaerobic conditions, ring-labeled 14C-
propham (test substance uncharacterized) declined from approximately
0.0 8 to approximately 0.04 ppm during 61 days of incubation in loam
soil in the dark at approximately 2 5°C and 60% of water holding
capacity (Hardies and Studer, 1979b); in sandy loam soil, the decline
was from approximately 0.06 to 0.0 3 ppm during 63 days of incubation
(Hardies and Studer, 1979c).
° 14c-Propham (purity unspecified) at 0.2 to 20 ppm was adsorbed to two
silt loams, a silty clay loam, a sandy clay loam, and two sandy loam
soils with Freundlich K values of 0.74 and 2.72, 1.77, 0.65, and 0.2 7
and 1.58, respectively (Hardies and Studer, 1979d). Ring-labeled
14c-propham (purity unspecified) was very mobile (>98% of applied
propham in leachate) in 30.5-cm columns of sandy clay loam and sandy loam
soil leached with 20 inches of water (Hardies and Studer, 1979e). It
was less mobile in columns of Babcock silt loam (42.3% in leachate),
silty clay loam (approximately 62% at 11- to 2 7-cm depth), and Wooster
silt loam (approximately 54% at 7.6- to 15-*nn depth) soils. Aged
(30-day) residues were relatively immobile in Wooster silt loam soil;
<1% of the applied radioactivity moved from the treated soil.
° Propham residues dissipated from the upper 6 inches of sandy loam,
sandy clay loam, silty loam, and silty clay loam field plots with
half-lives of 42 to 94, 57 to 160, 42 to 14 7, and approximately

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Propnam
August:, 1388
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21 to 42 days, respectively, following application of propham (ChemHoe
135^ 3 lb/gal F1C) at 4 and 8 lb active ingredient (a.i.) per acre
in September-November, 1977 (Pensyl and Wiedmann, 1979). Residues
were nondetectable (<0.02 ppm) within 164 to 283 days after treatment
at all rates and sites. In general, propham residues in the 6- to
12-inch depth were <0.04 ppm. Propham (3 lb/gal F1C) applied at
6 lb a.i./A in aid-May dissipated with a half-life of 10 to 15 days in
the 0- to 6-inch depth of silt loam soil (Wiedmann and Pensyl, 1981).
Ring-labeled 14c-propham (formulated as ChemHoe 135) applied at 4 lb
a.i./A dissipated with a half-life of <7 days in the upper 3 inches
of silt loam soil treated in November, 1981 (Wiedmann et al., 1982).
The second half-life occurred approximately 133 days post-treatment.
III. PHARMACOKINETICS
Absorption
•	After oral administration of 1,100 mg/kg 14C-isopropyl-labeled propham
(99% a.i.) to rats (1,100 mg/kg), 88% of the label appeared in urine
within 4 days. After oral doses of 1,100 mg/kg of 14C-phenyl-labeled
propham, 96% was excreted in urine and 2% was excreted in feces
(Chen, 1979).
•	Fang et al. (1972) reported that in rats given oral doses (ranging
from less than 4 mg/kg to 200 mg/kg) of 14C-propham (99% a.i.)
80 to 85% was excreted in urine and 5% was expired in air, indicating
that propham is well absorbed (85 to 98%) from the gastrointestinal
tract.
Distribution
0 Chen (1979) administered single oral doses of ^c-phenyl- or
14c-isopropyl-labeled propham (1,100 mg/kg 99% a.i.) to rats. Trace
amounts of both 14c-phenyl- or 14c-isopropyl-labeled (0.5 to 1.2%)
propham were present in the liver, kidneys, muscle and carcass after
48 hours.
0 Paulson and Jacobsen (1974) administered single oral doses of
14c-propham (100 mg/kg 99% a.i.) to goats. Six hours later,- only low
levels (0.2%) were detectable in milk.
Metabolism
0 Chen (1979) administered single oral doses of 14CT>henyl-labeled
propham (1,100 mg/kg 99% a.i.) to rats by gavage. Most of the dose
(96%) was excreted in urine as metabolites. The primary metabolites
identified were the sulfate ester conjugate and the glucuronide
conjugate of isopropyl 4-hydroxycarbanilate, which accounted for 73
and 1.3%, respectively, of the total primary metabolites recovered.
Similar studies in rats (single oral dose of 100 mg/kg) by Paulson
et al. (1972) support the rapid metabolism and excretion of propham.
In these studies a third metabolite (the sulfate ester of 4-hydroxy-

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August, 1983
acetanilide) and a fourth (unidentified) metabolite were found to
account for 12.3% and 8.9%, respectively, of the total metabolites
detected in urine. The data demonstrate that ring hydroxylation at
the 4-position and subsequent conjugation as well as hydrolysis and
subsequent tl-acetylation occurred prior to excretion.
Excretion
0 14c-Propham is rapidly excreted primarily in the urine of rats. Peak
urinary concentrations were reached 6 hours post-treatment. It was
found that 96% and 2% of the administered dose of 14c-propham (10 0
n»
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August /¦ 1 988
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Dermal/Ocular Effects
° The acute dermal LD5Q value in albino rabbits was reported to be
greater than 3,000 mg/kg (PPG Industries, 1978).
0 Propham (3% aqueous solution) was slightly irritating when applied to
the skin and eyes of albino rabbits (PPG Industries, 1978).
Long-term Exposure
• Tisdel et al. (1979) fed Sprague-Dawley rats (30/sex/dose) propham
(technical grade, purity not specified) in the diet at 0, 250, 1,000
or 2,000 ppm for 91 days. Assuming that 1 ppm in the diet of rats is
equivalent to 0.05 mg/kg/day (Lehman, 1959), these levels are equivalent
to 0, 12.5, 50 or 100 mg/kg/day. Following treatment, body weight,
organ weight, growth, clinical chemistry, gross pathology and histo-
pathology were evaluated. No effects were reported at 1,000 ppm
(50 mg/kg/day) or lower in any parameters measured. At the highest
dose (2,000 ppm or 100 mg/kg/day) there was a significant increase in
spleen weight (p <0.05) and in spleen-to-body weight ratio (p <0.01)
in males, and a 70% inhibition of plasma cholinesterase (p <0.01) in
females at 4 5 days. Based on the above data, a NOAEL of 1,000 ppm
(50 mg/kg/day) was identified.
Reproductive Effects
0 In a report of a three-generation rat reproduction study, Ravert
(1978) reported data from the P2 to weaning of the F2b generation.
Sprague-Dawley rats (10 males or 20 females/dose) were administered
technical grade propham (purity not specified) in the diet at dose
levels of 0, 87.5, 250, 750 or 1,500 ppm for 9 weeks prior to breeding
for each parental generation. Assuming that 1 ppm in the diet of
rats is equivalent to 0.0 5 mg/kg/day (Lehman, 1959), these levels are
equivalent to 0, 4.4, 12.5, 37.5 or 75 mg/kg/day. It was not clear
whether the test animals were also fed propham-^ontaining diets
during pregnancies or through weaning of offspring. No effects were
reported on fertility, mortality or pup development at any dose level
tested*
Developmental Effects
0 Ravert and Parke (1977) administered technical propham (purity not
specified) by gavage to pregnant Sprague-Dawley rats (16 to 20/dose),
at levels of 0, 37.6, 376 or 1,8 79 tng/kg/day on days 6 through
15 of gestation* End points that were monitored included maternal
and fetal body weight and the number of corpora lutea, implants, live
fetuses and dead fetuses. Fetuses were also examined for soft-tissue
and skeletal anomalies. The only effects detected were reduced
maternal and fetal body weights and higher resorption rates at the
highest dose tested (1,879 mg/kg) and increased incidences of incomplete
ossification of the parietal and frontal bones of the skull at 375.8
and 1,879 mg/kg. An apparent NOA£L appears to be 3 7.6 mg/kg/day.

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However, in this experiment, the high dose (1,879 mg/kg/day is too
high (i.e., one-half of the LD50); nearly two-thirds of the pregnant
rats at this dose died prior to scheduled sacrifice. Further, the dose
intervals are also relatively large. Therefore, a reliable NOAEL can
not be determined accurately due to the large difference in dosages
tested and the marginal effect noted at 376 mg/kg/day (For more
information on the developmental effects, see Worthing, 1979).
Mutagenicity
9 Using the Ames Salmonella test, Margard (1978) reported that propham
(purity not specified, 1,000 ug/plate) did not show any indications
of mutagenic activity either with or without activation.
* When propham (100 ug/mL, purity not specified) was applied to cultures
containing BALB/c 3T3 cell lines, no clonal transformation was evident
(Margard, 1978).
0 Friedrick and Nass (1983) reported that propham (1.1 to 2.2 mM) did
not induce mutation in S4 9 mouse lynphoma cells.
Carcinogenicity
8 Innes et al. (1969) administered propham to (C57BL/6 X C3H/ANf) or
(C7BL/6 X AKR) mice (18/sex) in the diet at 0 or 560 ppm for 18 months.
According to the author, this corresponds to a dose of about 0 to
215 mg/kg. The incidence of tumors was not significantly increased
(p >0.0 5) for any tumor type in any sex-strain subgroup or in the
combined sexes of either strain. This duration of exposure and this
dose level may not be sufficient for detecting late-occurring tumors.
0 Hueper (1952) fed 15 Osborne-Mendel rats (sex not specified) dietary
propham (20,000 ppm, purity not specified) for 18 months. The animals
were alternately placed from 1 to 2 months on the diet followed by
1 to 2 weeks on normal diet. Assuming that 1 ppm in the diet of rats
is equivalent to 0.05 mg/kg/day (Lehman, 1959), the dietary level was
equivalent to 1,000 mg/kg/day. The time-weighted average can not be
calculated due to a lack of detailed reporting of the study design.
No tumors were observed in 6 of 8 surviving rats that were evaluated
histologically. This study is limited by the low number of animals
used,' the poor survival rate, short duration, limited histopathological
examination and method of treatment.
0 Van Esch and Kroes (1972) fed groups of 23 to 26 golden hamsters 0 or
0.2% propham (2,000 ppm, purity not specified) in the diet for
33 months. Assuming that dietary assumptions appropriate for guinea
pigs are also appropriate for hamsters and that 1 ppm in the diet of
hamsters is equivalent to 0.04 mg/kg/day (Lehman, 1959), these levels
are equivalent to 0 or 80 mg/kg/day. Based on histological examination,
the authors reported no significant increase in tumor incidence.

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V. QUANTIFICATION OF TOXICOLOGICAL EFFECTS
Health Advisories (HAs) are generally determined for one-day, ten-day,
longer-term (up to 7 years) and lifetime exposures if adequate data are
available that identify a sensitive noncarcinogenic end point of toxicity.
The HAs for noncarcinogenic toxicants are derived using the following formula:
HA = (NOAEL or LOAEL) x (BW) = 	 mg/L (	 ug/L)
(UF) x (	 L/day)
where:
NOAEL or LOAEL = No- or Lowest-Observed-Adverse"Effect Level
in mg/kg bw/day.
BW = assumed body weight of a child (10 kg) or
an adult (70 kg).
UF = uncertainty factor (10, 100, 1,000 or 10,000),
in accordance with EPA or NAS/ODW guidelines.
	 L/day " assumed daily water consumption of a child
(1 L/day) or an adult (2 L/day).
One-day Health Advisory
No information was found in the available literature that was suitable
for determination of the One-day HA value for propham. It is, therefore,
recommended that the Longer-term HA value for a 10-kg child, 5 mg/L, calculated
below, be used at this time as a conservative estimate of the One-day HA value.
Ten-day Health Advisory
The Longer-term HA of 5 mg/L for a 10-kg child, calculated below, is
used for the Ten-day HA since the apparent NOAEL (37.6 mg/kg/day) in the
teratology study by Ravert and Parke (1977) was not necessarily the highest
NOAEL, due to the large difference between the doses selected (a ten-fold
difference between 37.6 and 376 mg/kg/day).
Longer-term Health Advisory
The study by Tisdel et al. (1979) has been selected to serve as the
basis for the Longer-^erm HA value for propham. In this study, rats were fed
propham in the diet for 91 days. At 100 mg/kg/day, plasma cholinesterase was
inhibited (70%) and spleen-to-body weight ratios were increased. No effects
were observed at 50 mg/kg/day. This NOAEL is supported by the NOAEL of 75
mg/kg/day identified in the three-generation reproduction study in rats by
'Ravert (1978).
Using a NOAEL of 50 mg/kg/day, the Longer-term HA for a 10-kg child is
calculated as follows:
Longer-term HA = (50 mg/kg/day) (10 kg) =5.0 mg/L (5,000 ug/L)
(100) (1 L/day)

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August, 1 988,
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where:
50 mg/kg/day = NOAEL, based on the absence of inhibition of cholin-
esterase or effects on organ weights in rats fed
propham in the diet for 91 days.
10 kg a assumed body weight of a child.
100 = uncertainty factor, chosen in accordance with EPA
or NAS/OCW guidelines for use with a NOAEL from an
animal study.
1 L/day » assumed daily water consumption of a child.
The Longer-term HA for a 70-kg adult is calculated as follows:
50 mg/kg/day = NOAEL, based on the	absence of inhibition of cholin-
esterase or effects	on organ weights in rats fed
propham in the diet	for 91 days.
70 kg =» assumed body weight	of an adult.
100 » uncertainty factor,	chosen in accordance with EPA
or NAS/ODW guidelines for use with a NOAEL from an
animal study.
2 L/day ¦ assumed daily water	consumption of an adult.
Lifetime Health Advisory
The Lifetime HA represents that portion of an individual's total exposure
that is attributed to drinking water and is considered protective of noncar-
cinogenic adverse health effects over a lifetime exposure. The Lifetime HA
is derived in a three-step process. Step 1 determines the Reference Dose
(RfD), formerly called the Acceptable Daily Intake (ADI). The RfD is an esti-
mate of a daily exposure to the human population that is likely to be without
appreciable risk of deleterious effects over a lifetime, and is derived from
the NOAEL (or LOAEL), identified froo a chronic (or subchronic) study, divided
by an uncertainty factor(s). From the RfD, a Drinking Water Equivalent Level
(DWEL) can be determined (Step 2). A DWEL is a medium-specific (i.e., drinking
water) lifetime exposure level, assuming 100% exposure from that medium, at
which adverse, noncarcinogenic health affects would not be expected to occur.
The -DWEL is derived from the multiplication of the RfD by the assumed body
weight of an adult and divided by the assumed daily water consumption of an
adult. The Lifetime HA is determined m Step 3 by factoring in other sources
of exposure, the relative source contribution (RSC). The RSC from drinking
water is based on actual exposure data or, if data are not available, a
value of 20% is assumed. If the contiaiunt is classified as a Group A or B
Longer-term HA
a (50 mg/kg/day) (70 kg)
(100) (2 L/day)
17.5 mg/L (20,000 ug/L)
where:

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August, 1983
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carcxnogen, according to the Agency's classification scheme of carcinogenic
potential (U.S. EPA, 1986a)/ then caution should be exercised in assessing the
risks associated with lifetime exposure to this chemical.
No chronic study was found in the available literature that was suitable
for determination of the Lifetime HA value for propham. The chronic studies
by Innes et al. (1969), Hueper (1952) and Van Esch and Kroes (1972) did not
provide adequate data on noncarcinogenic end points. In the absence of
appropriate chronic data, the 91-day study by Tisdel et al. (1979), which
identified a NOAEL of 50 mg/kg/day and was selected to serve as the basis for
the Longer-^erm HA, has also been selected for deriving the Lifetime HA.
Using this study, the Lifetime HA is calculated as follows:
Step 1: Determination of the Reference Dose (RfD)
RfD = (50 mg/kg/day) q.02 mg/kg/day (rounded from
(1,000) (3)	0,017 mg/kg/day)
where:
50 mg/kg/day 3 NOAEL, based on the absence of any cholinesterase
inhibition or effects on organ weights in rats fed
propham in the diet for 91 days.
1,000 = uncertainty factor, chosen in accordance with EPA
or NAS/ODW guidelines for use with a NOAEL from an
animal study of less-than-lifetime duration.
3 = additional uncertainty factor. This factor is used
to account for a lack of adequate chronic toxicity
studies in the data base, preventing establishment
of the most sensitive toxicological end point.
Step 2: Determination of the Drinking Water Equivalent Level (DWEL)
DWEL - (0.017 mg/kg/day) (70 kg) . 0.595 mg/L (600 ug/L)
(2 L/day)
where:
0.017 mg/kg/day ** RfD.
70 kg ** assumed body weight of an adult.
2 L/day «¦ assumed daily water consumption of an adult.
Step 3: Determination of the Lifetime Health Advisory
Lifetime HA =¦ (0.595 mg/L) (20%) =» 0.12 mg/L (100 ug/L}

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August, 1983
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where:
0.595 mg/L = DWEL.
20% = assumed relative source contribution from water.
Evaluation of Carcinogenic Potential
0 The International Agency for Research on Cancer (IARC, 1976) evaluated
propham and concluded that the carcinogenic potential is currently
cannot be determined.
0 Applying the criteria described in EPA's guidelines for assessment
of carcinogenic risk (U.S. EPA, 1906a), propham may be classified
in Group 0: not classified. Thi3 category is for substances with
inadequate animal evidence of carcinogenicity.
VI. OTHER CRITERIA, GUIDANCE AND STANDARDS
° No information on other existing criteria, guidelines and standards
was found in the available literature.
VII. ANALYTICAL METHOD
0 Analysis of propham is done by Method #4 of the NPS survey methods,
"Determination of Pesticides m Groundwater by High Performance Liquid
Chromatography with an Ultraviolet Detector" (U.S. EPA, 1986b). In
this method a 1 liter sample is extracted with methylene chloride,
reduced to 5 ml with methanol substitution and analysis by HPLC with
a UV detector* The method is being validated in a single laboratory
and the estimated detection limit for propham is 0.75 ug/L.
VIII. TREATMENT TECHNOLOGIES
° Available data indicate that granular activated carbon (GAC) adsorption
will remove propham from water.
° Whittaker (1980) experimentally determined adsorption isotherms for
propham on GAC.
9 Whittaker (1980) reported the results of studies with GAC columns
operating under bench scale conditions. At a flow rate of
0.3 gal/min/sq ft and an empty bed contact time of 6 minutes, propham
breakthrough (when effluent concentration equals 10% of influent
concentration) occurred after 720 bed volumes (BV).
° In the same study, Whittaker (1980) reported the results for seven
propham bi-solute solutions when passed over the same GAC continuous -
flow column.

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* The studies cited above indicate that GAC adsorption is the most
promising treatment technique for the removal of propham from water.
However, selection of an individual technology or combinations of
technologies for propham removal from water must be based on a case-
by-case technical evaluation and an assessment of the economics
involved.

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REFERENCES
Brown, J.H. and P. Gross.* 1949. Acute toxicity study of isopropyl n-phenyl
carbamate. Unpublished 3tudy. MRID 00075264.
CHEMLAB. 1985. The Chemical Information System, CIS, Inc., Bethesda, MD.
Chen, Y. * 1979. Summary of animal metabolism of IPC. Uhpublished study.
MRID 00115438.
Cohen, S.Z. 1984. List of potential groundwater contaminants. Memorandum
to I. Pomerantz. Washington, D.C.: U.S. Environmental Protection Agency.
August 28.
Fang, S.C., E. Fallin, M.L. Montgomery et al.* 1972. Metabolic studies of
14C-labeled propham and chloropropham in female rats. unpublished study.
MRID 00037854.
Fang, S.C. and E. Fallin. 1974. Metabolic studies of 14c-labeled propham
and chloropropham in the female rat. Pe9t. Biochem. Physiol. 4:1-11.
Friedrick, U. and G. Mass. 1983. Evaluation of a nutation test using S4 9
mouse lymphoma cells and monitoring simultaneously the induction of
dexamethasone resistance, 6-thioguanine resistance and ouabain resistance.
Mutat. Res. 110:147-162.
Gusik, F.F.* 1976. Photolysis of carbon 14 ring-labeled isopropyl carbanilate
(IPC) in water. Uhpublished study received Sept. 17, 1979 under 748-224;
submitted by PPG Industries, Inc., Barberton, OH; CDL: 240988-C. MRID
00115466.
Hardies, D.E.* 1979. Metabolism of isopropyl carbanilate on a Wooster silt
loam soil: BR 21422. Uhpublished study received Sept. 17, 1979 under
748-224; submitted by PPG Industries, Inc., Barberton, OH; CDL:240988-1.
MRID 00115472.
Hardies, D.E. and D.Y. Studer.* 1979ft. Metabolism of isopropyl carbanilate
on a Woodburn silt loam soil: BR 21448. Uhpublished study received
Sept. 17, 1979 under 748-224; submitted by PPG Industries, Inc., Barberton
OH; CDL:240998-F. MRID 00115469.
Hardies, D.8. and D.Y. Studer.* 1979b. Metabolism of isopropyl carbanilate
on an Altvan loam soil: BR 21531. Uhpublished study received Sept. 17,
1979 under 748-224; submitted by PPG Industries, Inc., Barberton, OH;
CDL:240988-H. MRID 00115471.
Hardies, D.E. and D.Y. Studer.* 1979c. Metabolism of isopropyl carbanilate
on a Hanford sandy loam: BR 21566. Uhpublished study received
Sept. 17, 1979 under 748-224; submitted by PPG Industries, Inc., Barberton
OH; CDL:240988-G. MRID 00115470.
Hardies, D.E. and D.Y. Studer.* 1979d. Absorption of isopropyl carbanxlate
on five soil types: BR 21590. Unpunlished study received Sept. 17,
1979 under 748-224; submitted by PPG Industries, Inc., Barberton, OH;
CDL:240987-C. MRID 00038945.

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Hardies, D.E. and D.Y. Studer.* 1979e. A laboratory study of the leaching of
isopropyl carbanilate in soils. Uhpublished study prepared and submitted
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