August, 1987
PROPHAM
Health Advisory
Office of Drinking Water
U.S. Environmental Protection Agency
I. INTRODUCTION
Y
V\
The Health Advisory (HA) Program, sponsored by the Office of Drinking
jVj Water (ODW), provides information on the health effects, analytical method-
(u ology and treatment technology that would be useful in dealing with the
x 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,
i exposures based on data describing nohcarcinogenic end points of.toxicity.
Health Advisories do not quantitatively incorporate any potential carcinogenic
risk from such exposure. 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 and 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-hit, 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.
Because each model-is based on differing assumptions, the estimates that are
derived can differ by several orders of magnitude.
U.S. Environmental Protection
Library, Room 2404 FM-211-A
401 M Street, S.W.
Washington. DC 20460
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Propham
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II. GENERAL INFORMATION AND PROPERTIES
CAS No. 122.-42-9
Structural Formula
NTC-0-CH(CH3)2
H
Phenyl 1-methylethyl carbamate; isopropyl-N-phenylcarbamate
Synonyms
IPC; Aglrmin; Ban-Hoe; Beet-Kleen; Birgin; Chem-Hoe; Collavin;
Ortho grass killer; Premalox; Profam; Prophos; Tixit; Triherbide;
Tuberit; USAF d-9 (Meister, 1983).
Uses
0 Pre- and postemergence herbicide for control of weeds in alfalfa,
clover, flax, lettuce, safflower, spinach, sugarbeets, lentils and
peas and on fallow land (Meister, 1983).
Properties (Meister, 1983; Cohen, 1984; CHEMLAB, 1985; TDB, 1985)
Chemical Formula C-|oH13°2N
Molecular Weight- 179.21
Physical State (25°C) White crystals
Boiling Point (at 25 mm Hg)
Melting Point
Vapor Pressure (25°C)
Specific Gravity (20°C/20°C)
Water Solubility (25°C)
Log Octanol/Water Partition
Coefficient
Taste Threshold
Odor Threshold
Conversion Factor
Occurrence
0 Propham has been found in 2 of 431 surface water samples analyzed
and in 10 of 431 ground water samples (STORET, 1987). Samples were
collected at 107 surface water locations and 395 ground water locations.,
and propham was found in three states. The 85th percentile of all
non-zero samples was 2 ug/L in surface water and 10 ug/L in ground
water sources. The maximum concentration found in surface water was
2 ug/L, and in ground"" water' i' was* 1 0 -ug/L..
87°C
1.09
250 mg/L
1.22 (calculated)
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Environmental Fate
^'"""""""^^ rf
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 25°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.
0 Under aerobic conditions, ring-labeled ^c-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 25°C and 60% of water holding- capacity.
0 Under anaerobic conditions, ring-labeled ^4C-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 25°C arid 60% of water holding capacity (Hardies 1979; Hardies
and Studer, 1979a). Under, anaerobic conditions, ring-labeled 14C- ..
propham (test substance uncharacterized) declined from approximately
0.08 to approximately 0.04 ppm during 61 days of incubation in loam
soil in the'dark at approximately 25°C and 60% of water holding
capacity (Hardies and Studer, T979b); in sandy .loam soil, the decline
was from approximately 0.06 to 0.03 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 0.27
and 1.58, respectively '(Hardies and Studer, 1979d). Ring-labeled
14c-propham (purity unspecified) wag 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 27-cm depth), and Wooster
silt loam (approximately 54% at 7.6- to 15-cm 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
halfrlives of 42 to 94, 57 to 160, 42 to 147, and approximately
21 to 42 days, respectively, following application of propham (ChemHoe
135, 3 Ib/gal F1C) at 4 and 8 Ib active ingredient (a.i.) per acre
in September-November, 1977 (Pensyl and Wiedmahn, 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 Ib/gal P1C) applied at
6 Ib a.i./A in mid-May dissipated with a half-life of 10 to 15 days in
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Propham
August, 1987
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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 Ib
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 ^4C-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
.Chen (1979) administered single oral doses of 14C-phenyl- or
1^C-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.
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.
v...
Metabolism
Chen (1979) administered single oral doses of 14C-phenyl-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 78
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-
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 IJ-acetylation occurred prior to excretion.
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Propham August, 1987
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u
Excretion
14c-proph~am 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°
mg/kg 99% a.i.) was excreted in the urine and feces, respectively (Chen,
1979; Paulson et al., 1972).
Fang et al. (1972) reported that after oral administration of ring-
.or chain-14C-labeled propham (99% a.i.) to rats, 80 'to 85% of the
administered dose was excreted in the urine over a 3-day period. In
animals dosed with 14c-isopropyl-labeled propham, 5% was detected as
expired carbon dioxide.
IV. HEALTH EFFECTS
Humans
No information was found in the available literature on the health
effects of propham in humans.
Animals
Short-term Exposure t .
* Terrell and Parke (1977) administered single oral doses of propham
(technical grade, purity not specified) to groups of 10 male and 10
female rats and monitored adverse effects for "14 days. Doses of
2,000'mg/kg produced loss of righting reflex, ptosis, piloerection,
decreased locomotor activity, chronic pulmonary disease and rugation
and irregular thickening of the stomach. The acute oral LDSQ values
in male and female rats were reported to be 3,000 ± 232 mg/kg and
2,360 ±118 mg/kg, respectively. A No-ObservedrAdverse-Effeet-Level
(NOAEL) cannot be derived from the study because the doses used were
too high, and adverse effects were found at all doses tested.
0 Brown and Gross (1949) reported that when a single dose of 1,140
mg/kg propham (purity riot specified)- was administered orally to rats
(number not specified), no adverse effects were observed. Doses of
2,200 to 3,320 mg/kg resulted in periods of light anesthesia. Deep
anesthesia was produced when 4/420 mg/kg of propham ^ras administered,
with subsequent death of 38% of the test animals. ~
0 The acute inhalation LC5Q -value in albino rats was reported to
be 10.71 mg/L (PPG Industries, 1978).
Dermal/Ocular Effects -J
0 The acute dermal 1050 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).
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Propham August, 1987
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Long-term Exposure
0 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 45 days. Based on" the above data, a NQAEL 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 ?2 to weaning of the F2j> 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 0.05 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-containing 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 1,879 mg/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 NOAEL appears to be 37.6 mg/kg/day.
However, in this experiment, the high dose (1,879 mg/kg/day is too
high (i.e., one-half of the LDso); 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).
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Propham August, 1987
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Mutagenicity
0 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.
0 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 S49 mouse lymphoma cells.
Carcinogenieity
°" Innes et al. (1969) administered propham to C57BL/6XC3H/AMF or
C57BL/6XAKR mice (18/sex) in the diet at 560 ppm for 18 months.
Assuming that 1 ppm in the diet of mice is equivalent to 0.15 mg/kg/day
(Lehman, 1959), this corresponds to a dose of about 84 mg/kg/day.
The incidence'of tumors was not significantly increased (p >0.05)
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
r-x propham (20,000 ppm, purity hot 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 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.
V. QUANTIFICATION OF TOXICOLOGICAL EFFECTS
Health Advisories (HAs) are generally determined for one-day, ten-day,
longer-term (approximately 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 = JNOAEL' or LOAEL) X (BW) = mg/L ( ug/L)
(UP) x.( L/day)
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Propham August, 1987
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where:
NOAEL or LOAEL = No- or Lowest-Observed-Adverse-Eff ect-Level
in mg/kg bw/day.
BW = assumed body weight of a child (10 kg) or
an adult (70 kg).
OF < uncertainty factor (10, 100 or 1,000), in
accordance with 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 Ten-day HA value for a 10-kg child, 5 mg/L, 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 10-day HA because 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-term 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
ing/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:
V
where:
Longer-term HA « (5° "W/Jw/day) (10 kg) , 5<0 /L (5 000 ug/L)
(100) (1 L/day) y
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 = assumed body weight of a child.
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Propham .... ' August, 1987
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' *M ' ? V' v ;:.'< 2
. ' ' . . I '. ..
, . ~f ' , <<,', 1
1 00 = uncertainty' factor, chosen in accordance with NAS/ODW
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:
>
Longer-term HA = '(50 ;mg/kg>day) (70 kg) "1*7.5 mg/L (17,500 ug/L)
(100) (2.L/day)
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.
70 kg = assumed body weight of an adult.
100 = uncertainty factor, chosen in accordance with 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 from 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 effects 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 in 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 for synthetic organic chemicals and a value of 10%
is assumed for inorganic chemicals. If the contaminant is classified as a
Group A or B carcinogen, 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 90rday study by Tisdel et al. (1979), which
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Propham August, 1987
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identified a NOAEL of 50 mg/kg/day and was selected to serve as the basis for
the Longer-term 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) = 0.017 mg/kg/day
(1,000) (3)
where:
50 mg/kg/day = 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 NAS/ODW
guidelines for use with a NOAEL from an animal study
of less-than-lifetime duration.
3 = additional uncertainty factor used in the Office of
Pesticide Programs (OPP) Guidance for Establishing RfD
dated May 1, 1987 as an Addendum to TOX SOP #1002).
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 (595 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 (120 ug/L)
where:
0.595 mg/L = DWEL.
20% » assumed relative source contribution from water.
Evaluation of Carcinogenic Potential
i
0 The International Agency for Research on Cancer (IARC, 1976) evaluated
propham and concluded that the carcinogenic potential is indeterminate.
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Propham August, 1987
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0 Applying the criteria described in EPA's guidelines for assessment
of carcinogenic-risk (U.S. EPA, 1986a), propham may be classified
in Group D: not classified. This category is for substances with
inadequate animal evidence of carcinogenic!ty.
VI. OTHER CRITERIA, GUIDANCEAND STANDARDS
0 No information on other existing criteria, guidelines and standards
was found in the available literature.
VII. ANALYTICAL. METHODS
0 -Analysis of propham is. by a high-performance liquid chromatographic
(HPLC) method applicable to the determination-iof certain carbamate
and urea pesticides in water samples (U.S., EPA,. 1986b); This, method
requires a solvent extraction of approximately 1 L of sample with
-methylene chloride using a separatory funnel. ' The methylene chloride
extract is dried and concentrated to a.volume of.10 mL or less.
Compounds are separated by HPLC, and measurement is conducted with a
UV detector. The method detection limit has not been determined for .
propham, but it is estimated that the detection limits for analytes
included in this method are in the range of 1 to 5 ug/L.
VIII. TREATMENT TECHNOLOGIES . . . . - .
0 Available data indicate that granular activated carbon (GAG) adsorption
will remove propham from water.
0 Whittaker (1980) experimentally determined adsorption isotherms for
propham on GAG. - .
0 Whittaker (1980) reported the results of .studies with GAG columns
operating under bench scale conditions. At a flow rate of
0*8 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).
0 In the same study, Whittaker (1980) reported the results for seven
propham bi-solute solutions when passed over the same GAG continuous-
flow column. -.-... -.
0 The studies cited above indicate that GAG adsorption ia the most
promising treatment technique for the removal of propham from water.
However, selection of individual 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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Propham - August, 1987
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IX. REFERENCES
Brown, J.H. and P. Gross.* 1949. Acute toxicity .study of isopropyl n-phenyl
carbamate. Unpublished study. MRID 00075264.
CHEMLAB, 1985. Hie Chemical Information System, CIS, Inc., Bethesda, MD.
Chen, Y.* 1979. Summary of animal metabolism of IPC. Unpublished study.
MRID 00115438.
Cohen, S.2. 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
1^-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 chlorophropham in the female rat. Pest. Biochem. Physiol. 4:1-11.
Friedrick, U. and G. Nass. 1983. Evaluation of a mutation test using S49
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. Unpublished study received Sept. 17, 1979 under 748-224; --
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Propham - August, 1987
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>
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