DRAFT
August, 1987
P"°R 820K88110
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.
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.
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Propachlor
August, 1987
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II. GENERAL INFORMATION AND PROPERTIES
CAS No. 1918-16-7
Structural Formula
CH(CH3}2
COCH2C1
2-chloro-N-i sopropylacetinilide
Synonyms
0 Bexton; Prolex; Ramrod (Meister, 1983).
Uses
8 Selective postemergence herbicide used for control of many grasses
and certain broadleaf weeds (Meister, 1983).
Properties (Rao and Davidson, 1982; HSDB, 1986)
Chemical Formula
Molecular Weight
Physical State (room temp.)
Boiling Point
Melting Point
Density (25°C)
Vapor Pressure
Specific Gravity
Water Solubility (20°C)
Log Octanol/Water Partition
Coefficient
Taste Threshold
Odor Threshold
Conversion Factor
CnH14ClNO
211.69
White crystalline solid
110°C at 0.03 mm HG
67 to 76°C
1.13 g/mL
2.3 x 10-4 mm Hg
700 mg/L
1.61
Occurrence
Propachlor has been found in 132 of 1,144 surface water samples
analyzed and in 2 of 76 ground water samples (STORET, 1987). Samples
were collected at 314 surface water locations and 94 ground water
locations, and propachlor was found in eight states. The 85th
percentile of all nonzero samples was 2 ug/L in surface water and
0«12 ug/L in ground water sources. The maximum concentration found
was 10 ug/L in surface water and 0.12 ug/L in ground water.
Environmental Fate
Propachlor is degraded in aerobic soils in the laboratory and in the
field with half-lives of 2 to approximately 14 days, when the soils
are treated with propachlor at recommended application rates. However,
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Propachlor August, 1987
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degradation was relatively slower in soil treated at 500 ppm, and 90%
of the applied material remained after 21 days (Registrant CBI data).
0 The major propachlor degradates produced under aerobic soil conditions
are [ (1-methylethyl)phenylamino]oxoacetic acid and [ (2-methylethyD-
phenylamino]-2-oxoethane sulfonic acid. These degradates are recalci-
trant to further degradation in soil under anaerobic conditions. The
half-life of propachlor in anaerobic soil is <4 days (Registrant CBI
data).
0 Propachlor degrades very slowly (84.5% remaining after 30 days) in
lake water (Registrant CBI data).
0 Propachlor is moderately mobile to very mobile in soils ranging in
texture from sand to clay. Mobility appears to be correlated with
clay content and to a lesser degree with organic matter content and
CEC. Aged 14c-propachlor residues were mobile in a silt loam soil
(Registrant CBI data).
0 The rapid degradation of low levels of propachlor in soils is expected
to result in a low potential for groundwater contamination by propachlor
degradates. 1^C-Propachlor residues are taken up by rotated corn
planted under confined conditions; <3% of the radioactivity remained
in soil at the time of planting (Registrant CBI data).
III. PHARMACOKINETICS
Absorption
0 No direct data on rate of gastrointestinal absorption of propachlor
were found in the available literature. Based on recovery studies,
propachlor appears to be rapidly absorbed by the oral route of admin-
istration. An estimated 68% of a single dose of 10 mg of ring-labeled
14-c propachlor administered to 12 rats was recovered in urine 56
hours after compound administration (Malik, 1986). These results are
supported by other studies in which 54 to 64% (Lamoureux and Davison,
1975) and 68.8% (Bakke et al., 1980) of the administered dose was
recovered in urine 24 hours and 48 hours after dose administration,
respectively.
Distribution
0 Fifty-six hours following oral administration of 10 mg of ring-
labeled 14C-propachlor (purity not specified) to rats, no detectable
levels of radioactivity were identified in any tissue samples (Malik,
1986).
Metabolism
8 Metabolism of propachlor occurs by initial glutathione conjugation
followed by conversion via the mercapturic acid pathway; oxidative
metabolism also occurs (Lamoureux and Davison, 1975; Malik, 1986).
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Propachlor August, 1987
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Eleven urinary metabolites have been identified as the result of
propachlor metabolism in rats. The primary metabolic end products
of propachlor are mercapturic acid and glucuronic acid conjugates
(approximately 20 to 25%), methyl sulfones (30 to 35%), and phenols
and alcohols (Lamoureux and Davison, 1975; Malik, 1986).
Excretion
Propachlor (purity not specified) was excreted in the form of metabo-
lites in the urine (68%) and feces (19%) of rats within 56 hours after
dosing with ring-labeled 14c-propachlor. Methyl sulfonyl metabolites
accounted for 30 to 35% of the administered dose (Malik, 1986).
In studies with germ-free rats, 98.6% of the administered dose (not
specified) for propachlor (purity not specified) was identified in
the urine (68.8%) and feces (32.1%) within 48 hours. The major
metabolite was mercapturic acid conjugate, which accounted for 66.8%
of the administered dose (Bakke et al., 1980).
IV. HEALTH EFFECTS
Humans
Schubert (1979) reported a case study in which occupational exposure
to propachlor for 8 days resulted in erythemato-papulous (red pimply)
contact eczema on the hands and forearms.
Animals
Short-term Exposure
0 The acute oral LD5Q values for technical-grade (approximately 96.5%)
and wettable powder (WP) (65%) propachlor range from 1,200 to 4,000
mg/kg in rats. Technical-grade and wettable powder propachlor both
produced a low LD^Q value of 1,200 mg/kg (Keeler et al., 1976;
Heenehan et al., 1979; Auletta and Rinehart, 1979; Monsanto, (undated),
0 Beagle dogs (two/sex/dose) were administered propachlor (65% WP) in
the diet for 90 days at dose levels of 0, 1.3, 13.3 or 133.3 mg/kg/day
(Wazeter et al.. 1964). Body weight, survival rates, food consump-
tion, behavior, general appearance, hematology, biochemical indices,
urinalysis, histopathology and gross pathology were comparable in
treated and control animals. The No-Observed-Adverse-Effect-Level
(NOAEL) identified for this study is 133.3 mg/kg/day (the highest
dose tested).
0 Naylor and Ruecker (1985) fed propachlor [96.1% active ingredient
(a.i.)3 to beagle dogs {six/sex/dose) in the diet for 90 days at dose
levels of 0, 100, 500 or 1,500 ppm. Based on the assumption that
1 ppm in food is equivalent to 0.025 mg/kg/day (Lehman, 1959), these
doses are equivalent to 0, 2.5, 12.5 or 37.5 mg/kg/day. Clinical
signs, ophthalmoscopic, clinicopathologic, gross pathology and
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Propachlor August, 1987
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histopathologic effects were comparable for treated and control
groups. The reduction in food consumption and concomitant reductions
in body weight gain at all test levels were considered by the author
to be due to poor diet palatability. Based on these responses, a
NOAEL of 1,500 ppm (37.5 mg/kg/day) was identified.
Dermal/Ocular Effects
0 The acute dermal LD5Q value of technical propachlor and WP (65% propa-
chlor) in the rabbit ranges from 380 rag/kg to 20 g/kg (Keeler et al.,
1976; Monsanto, undated; Braun and Rinehart, 1978). Wettable powder
produced the lowest LD50 in rabbits (380 mg/kg); the lowest LD5Q produced
by technical propachlor was between 1,000 and 1,260 mg/kg in rabbits.
0 Propachlor (94.5% a.i.) (1 g/mL) applied to abraded and intact skin
of New Zealand White rabbits (three/sex) for 24 hours produced erythema
and slight edema at treated sites 72 hours post-treatment (Heenehan
et al., 1979).
0 Heenehan et al. (1979) instilled single applications (0.1 cc) of
propachlor into one eye of tested New Zealand rabbits for 30 seconds.
Corneal opacity with stippling and ulceration, slight iris irritation,
conjunctival redness, chemosis, discharge and necrosis were reported
at 14 days. Similar responses were reported by Keeler et al. (1976)
for a corresponding observation period and by Auletta (1984) during
3 to 21 days post-treatment.
Long-term Exposure
0 Albino rats (25/sex/dose) administered 0, 1.3, 13.3 or 133.3 mg/kg/day
propachlor (65% WP = 65% a.i.) in the diet for 90 days showed decreased
weight gain (10 to 12% less than control levels) in and increased
liver weights in both sexes (10% greater than control levels) at
133.3 mg/kg/day (the highest dose tested) (Wazeter et al., 1964).
The body and liver weights of rats of both sexes that received the
low dose and mid dose were comparable to control levels. Survival,
biochemical indices, hematology, urinalysis, gross pathology and
histopathology did not differ significantly between treated and
control groups. The NOAEL identified in this study is 13.3 mg/kg/day.
The Lowest-Observed-Adverse-Effect-Level (LOAEL) is 133.3 mg/kg/day
(the highest dose tested).
0 Reyna et al. (1984a) administered propachlor (96.1% a.i.) to rats
(30/sex/dose) in the diet for 90 days at mean dose levels of 0, 240,
1,100 or 6,200 ppm. Assuming that 1 ppm is equivalent to 0.05 mg/kg/day,
these concentrations correspond to 0, 12, 55 or 310 mg/kg/day (Lehman,
1959). Body weights and food consumption were significantly decreased
(no p value specified) at 55 mg/kg/day and 310 mg/kg/day in both
sexes. Final body weights for females were 7 and 36% less than
controls at the mid- and high-dose levels, respectively. In males,
final body weights were 8 and 59% less than control levels for mid-
and high-dose levels, respectively. However, histopathological
examination showed no changes. Mid- and high-dose levels produced
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Propachlor August, 1987
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increased platelet counts, decreased white blood cell counts and mild
liver cell dysfunction. Mild hypochromic, microcytic anemia was
reported at the high dose. A NOAEL of 12 mg/kg/day can be identified
for this study.
0 Albino mice {30/sex/dose) were fed propachlor (96.1% a.i.) in the
diet for 90 days at mean dose levels of 0, 385, 1,121 or 3,861 ppm
(Reyna et al., 1984b). Based on the assumption that 1 ppm in food
is equivalent to 0.15 mg/kg/day (Lehman, 1959), these doses correspond
to 0, 58, 168 or 579 mg/kg/day. Reduced body weight gain, decreased
white blood cell count, liver and kidney weight changes and increased
incidences of centrolobular hepatocellular enlargement were reported
at the mid (168 mg/kg/day) and high (579 mg/kg/day) doses when
compared to controls. Based on these responses, a NOAEL of 385 ppm
(58 mg/kg/day) can be identified.
Reproductive Effects
0 No information on the reproductive effects of propachlor was found in
the available literature.
Developmental Effects
0 Miller (1983) reported no signs of maternal toxicity in New Zealand
female rabbits (16/dose) that were administered propachlor (96.5%)
orally by gavage at doses of 0, 5, 15 or 50 mg/kg/day on days 7 to 19
of gestation. Statistically significant increases in mean implantation^
loss with corresponding decreases in the mean number of viable fetuses
were reported at 15 and 50 mg/kg/day when compared to controls. Two
low-dose and one mid-dose rabbit aborted on gestation days 22 to 25.
These effects, however, do not appear to be treatment-related since
no abortions occurred in the high-dose animals. No treatment-related
effects were present in the 5-mg/kg/day group (the lowest dose tested).
The authors reported that the maternal and embryonic NOAELs were 50
and 5 mg/kg/day, respectively.
8 Schardein et al. (1982) administered technical propachlor orally by
gavage to rats (25/dose) at dose levels of 0, 20, 60 or 200 mg/kg/day
during days 6 to 19 of gestation. There were no adverse fetotoxic or
maternal effects reported at any dose level. Based on this information,
the NOAEL identified in this study was 200 mg/kg/day (the highest
dose tested).
Mutagenicity
0 Technical propachlor was not genotoxic in assays of Salmonella
typhimurium with or without plant and animal activation; however,
genotoxic activity was reported in yeast assays (Saccharomyces
cerevisiae) at 1.3 x 10~3 M and 3 mg per plate after plant activation
(Plewa et al., 1984).
0 In a cytogenic study, propachlor administered for 24 hours by intra-
peritoneal injection at dose levels of 0.05, 0.2 or 1.0 mg/kg to F344
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Propachlor August, 1987
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rats did not induce chromosomal aberrations in bone marrow cells
(Ernst and Blazak, 1985).
0 Gene mutation was not detected in assays employing Chinese Hamster
Ovary (CHO) cells. Primary rat hepatocytes exposed to 1,000 and
5,000 ug/mL technical-grade propachlor showed no effect on unscheduled
DNA synthesis when compared to controls (Flowers, 1985; Steinmetz and
Mirsalis, 1984).
Carcinogenicity
0 No information was found in the available literature to evaluate the
carcinogenic potential of propachlor. However, several chemicals
analogous to this compound, i.e., alachlor and acetochlor, were found
to be oncogenic in two animal species.
V. QUANTIFICATION OFTOXICOLOGICAL 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 follpwing 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 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 propachlor. It is therefore
recommended that the Ten-day HA value for the 10-kg child (0.5 mg/L, calculated
below) be used at this time as a conservative estimate of the One-day HA value.
Ten-day Health Advisory
The developmental toxicity study in rabbits by Miller (1983) has been
selected as.the basis for determination of the Ten-day HA value for propachlor.
Pregnant rabbits administered propachlor (96.5%) by gavage at a dose level of
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Propachlor August, 1987
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5 mg/kg/day showed no clinical signs of toxicity in the adult animals and no
reproductive or developmental effects in the fetuses. The study identified a
NOAEL of 5 mg/kg/day. These results are supported by a reproduction study
reported by Schardein et al. (1982) in which rats were administered doses
ranging from 20 to 200 mg/kg/day during gestation, with no adverse fetotoxic
or maternal effects reported at any dose level. The NOAEL identified in that
study was 200 mg/kg/day (the highest dose tested). However, since the rabbit
appears to be the more sensitive species, the NOAEL identified in the rabbit
study will be used to derive the Ten-day HA.
Using a NOAEL of 5 mg/kg/day, the Ten-day HA for a 10-kg child is
calculated as follows:
Ten-day HA = (5 mg/kg/day) (10 kg) = 0.5 mg/L (500 ug/L)
(100) (1 L/day)
where?
5 mg/kg/day = NOAEL, based on the absence of clinical signs of toxicity
and the lack of reproductive or teratogenic effects in
rabbits exposed to propachlor by gavage for 12 days
during gestation.
10 kg = assumed body weight of a child.
100 = 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.
Longer-term Health Advisory
Because no suitable long-term studies were available to calculate a
Longer-term HA, it was decided that it would be more appropriate to use the
Reference Dose of 0.013 mg/kg/day and adjusting this number to protect a
10-kg child and a 70-kg adult. The resulting Longer-term HA thus becomes
0.13 mg/L and 0.46 mg/L for a 10-kg child and a 70-kg adult, respectively.
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
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Propachlor August, 1987
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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, 1986), then caution should be exercised in
assessing the risks associated with lifetime exposure to this chemical.
The 90-day study by Wazeter et al. (1964) has been selected to serve as
the basis for determination of the Lifetime HA value for propachlor. Based
on body and liver weight effects, a NOAEL of 13.3 mg/kg/day was identified.
These results were further verified by the results of a similar study with
rats conducted by Reyna et al. (1984a) in which a NOAEL of 12 mg/kg/day was
identified.
Step 1: Determination of the Reference Dose (RfD)
RfD = (13.3 mg/kg/day) _ Q.013 mg/kg/day
(1,000)
where:
13.3 mg/kg/day = NOAEL based on the absence of effects on body weight
and liver weight in rats exposed to propachlor for
90 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.
Step 2: Determination of the Drinking Water Level (DWEL)
DWEL = (0.013 mg/kg/day) (70 kg) , 0>46 /L (460 /L)
(2 L/day)
where:
0.013 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 = (0.46 mg/L) (20%) = 0.092 mg/L (92 ug/L)
where:
0.46 mg/L = DWEL.
20% = assumed relative source contribution from water.
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Propachlor August, 1987
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Evaluation of Carcinogenic Potential
0 No studies on the carcinogenic potential of propachlor were found in
the available literature. However, other structurally similar compounds
such as alachlor and acetochlor have been found to be potent carcinogens.
0 Applying the criteria described in EPA's final guidelines for assessment
of carcinogenic risk (U.S. EPA, 1986), propachlor may be classified
in Group D: not classified. This category is for substances with
inadequate human and animal evidence of carcinogenicity.
VI. OTHER CRITERIA, GUIDANCE AND STANDARDS
0 Residue tolerances ranging from 0.02 to 10.0 ppm have been established
for propachlor in or on agricultural commodities (U.S. EPA, 1985).
0 NAS (1977) has recommended an ADI of 0.1 mg/kg/day and a Suggested-
No-Adverse-Effect Level (SNARL) of 0.7 mg/L, based on a NOAEL of
100 mg/kg/day in a rat study (duration of study not available).
VII. ANALYTICAL METHODS
(to be provided by STB)
VIII. TREATMENT TECHNOLOGIES
No data were found for the removal of propachlor from drinking water
by conventional treatment or by activated carbon treatment.
0 No data were found for the removal of propachlor from drinking water
by aeration. However, the Henry's Coefficient can be estimated from
available data on solubility (700 mg/L at 20°C) and vapor pressure
(2.3 x 1Q~4 mm Hg at 25°C). Propachlor probably would not be amenable
to aeration or air stripping because its Henry's Coefficient is
approximately 0.0051 atm. Baker and Johnson (1984) reported the
results of water and pesticide volatilization from a waste disposal
pit. Over a 2-year period, approximately 66.4 mg of propachlor
evaporated for every liter of water which evapoz*ted and only 8.3%
of the propachlor was removed. These results support the assumption
that aeration would not effectively remove propachlor from drinking
water.
0 Propachlor is similar in structure to alachlor and has similar physical
properties. The effectiveness of various processes for removing
propachlor would probably be similar to that of alachlor.
0 Alachlor is amenable to the following processes:
- GAC (Miltner and Fronk, 1985; DeFilippi et al., 1980).
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Propachlor August, 1987
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- PAC (Miltner and Fronk, 1985; Baker, 1983).
Ozonation (Miltner and Fronk, 1985).
Reverse osmosis (Miltner and Fronk, 1985).
0 Chlorine and chlorine dioxide oxidation were partially effective in
removing alachlor from drinking water (Miltner and Fronk, 1985).
0 The following processes were not effective in removing alachlor from
drinking water:
Diffused aeration (Miltner and Fronk, 1985).
Potassium permanganate oxidation (Miltner and Fronk, 1985).
Hydrogen peroxide oxidation (Miltner and Fronk, 1985).
- Conventional treatment (Miltner and Fronk, 1985; Baker, 1983).
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Propachlor August, 1987
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IX. REFERENCES
Auletta, C., and W. Rinehart.* 1979. Acute oral toxicity in rats: Project No.
4891-77, BDN-77-431. Unpublished study. MRID 104342.
Auletta, C.* 1984. Eye irritation study in rabbits. Propachlor. Project No.
5050-84. Unpublished study. Biodynamics, Inc. MRID 151787.
Baker, D. 1983. Herbicide contamination in municipal water supplies in
northwestern Ohio. Final draft report. Prepared for Great Lakes National
Program Office, U.S. Environmental Protection Agency, Tiffin, OH.
Baker, J.L., and L.A. Johnson. 1984. Water and pesticide volatilization
from a waste disposal pit. Transactions of the American Society of
Agricultural Engineers. 27:809-816. May/June.
Bakke, J., J. Gustafsson and B. Gustafsson. 1980. Metabolism of propachlor
by the germ-free rat. Science. 210:433-435. October.
Braun, W., and W. Rinehart.* 1978. Acute dermal toxicity in rabbits [due to
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430. Unpublished study. MRID 104351.
DeFilippi, R.P., V.J. Kyukonis, R.J. Robey and M. Modell. 1980. Super-
critical fluid regeneration of activated carbon for adsorption of
pesticides. Research Triangle Park, U.S. Environmental Protection
Agency. EPA-600/2-80-054.
Ernst, T., and W. Blazak.* 1985. An assessment of the mutagenic potential of
propachlor utilizing the acute in vivo rat bone marrow cytogenetics assay
(SR 84-180): Final Report: SRI Project LSC-7405. SRI International.
Unpublished study. MRID 00153940.
Flowers, L.* 1985. CHO/HGPRT gene mutation assay with propachlor: Final
Report: EWL 840083. Unpublished study. MRID 00153939.
Heenehan, P., W. Rinehart and W. Braun.* 1979. Acute oral toxicity study in
rats. Project No. 4887-77. BDN-77-430. Biodynamics, Inc. MRID 104350C
HSDB. 1986. Hazardous Substances Database. National Library of Medicine,
Bethesda, MD.
Keeler, P.A., D.J. Wroblewski and R.J. Kociba.* 1976. Acute toxicological
properties and industrial handling. Hazards of technical grade propachlor•
Unpublished study. MRID 54786.
Lamoureaux, G., and K. Davison.* 1975. Mercapturic acid formation in the
metabolism of propachlor, CDAA, Fluorodifen in the rats. Pesticide
Biochem. Physiol. 5:497-506.
Lehman, A.J. 1959. Appraisal of the safety of chemicals in foods, drugs and
cosmetics. Assoc. Food Drug Off. U.S., Q. Bull.
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Propachlor August, 1987
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Malik, J.* 1986. Metabolism of propachlor in rats: Report No. MSL-5455;
Job/Project No. 7815 (Summary). Unpublished study. MRID 157495.
Meister, R., ed. 1983. Farm chemicals handbook. Willoughby, OH: Meister
Publishing Company.
Miller, L.* 1983. Teratology study in rabbits {IR-82-224):401-190. Inter-
national Research and Development Corporation. Unpublished study.
MRID 00150936.
Miltner, R.J., and C.A. Fronk. 1985. Treatment of synthetic organic contami-
nants for Phase II regulations. Internal report. U.S. Environmental
Protection Agency, Drinking Water Research Division. December.
Monsanto Company.* Undated. Toxicology. Summary of studies 241666-C through
241666-E. Unpublished study. MRID 25527.
NAS. 1977. National Academy of Sciences. Drinking water and health.
Washington, DC: National Academy Press.
Naylor, M., and F. Ruecker.* 1985. Subchronic study of propachlor admini-
stered in feed to dogs: DMEH Project No. ML-84-092. Unpublished study.
MRID 00157852.
Plewa, M.J., et al. 1984. An evaluation of the genotoxic properties of herbi-
cides following plant and animal activation. Mutat. Res. 136(3):233-246.
Rao, P.S.C., and J.M. Davidson. 1982. Retention and transformation of
selected pesticides and phosphorus in soil-water systems: A critical
review. U.S. EPA, Athens, GA. EPA-600/53-82-060.
Reyna, M., W. Ribelin, D. Thake et al.* 1984a. Three month feeding study of
propachlor to albino rats: Project No. ML-83-083. Unpublished study.
MRID 00152151.
Reyna, M., W. Ribelin, D. Thake et al.* 1984b. Three month feeding study of
propachlor to albino rats: Project No. ML-81-72. Unpublished study.
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