August, 1987 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. 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. ------- Propham August, 1987 -2- II. GENERAL INFORMATION AND PROPERTIES CAS No. 122.-42-9 Structural Formula 0 N-C-0-CH(CH3)2 H Phenyl 1-methylethyl carbamate; isopropyl-N-phenylcarbamate Synonyms 0 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 C10H13°2N Molecular Weight 179.21 Physical State (25°C) White crystals Boiling Point (at 25 mm Hg) — Melting Point 87°C Vapor Pressure (25°C) Specific Gravity (20°C/20°C) 1.09 Water Solubility (25°C) 250 mg/L Log Octanol/Water Partition 1.22 (calculated) 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 it was 10 ug/L. ------- Prophara August, 1987 -3- 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 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 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 25°C and 60% of water holding capacity. 0 Under anaerobic conditions, ring-labeled I^C-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 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 0.08 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, 1979b); in sandy loam soil, the decline was from approximately 0.06 to 0.03 ppm during 63 days of incubation (Hardies and Studer, 1979c). 0 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 1 'kVpropham (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 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. 0 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 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 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 Ib/gal F1C) applied at 6 Ib a.i./A in mid-May dissipated with a half-life of 10 to 15 days in ------- Propham August, 1987 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 , 1 00 mg/kg 1 4C-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 1 4C-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 Chen. (1979) administered single oral doses of 14C-phenyl- or 1 4C-isopropyl-labeled propham (1,100 mg/kg 99% a.i.) to rats. Trace amounts of both 1 ^-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 1 4C -propham (100 mg/kg 99% a.i.) to goats. Six hours later, only low levels (0.2%) were detectable in milk. Metabolism Chen (1979) administered single oral doses of 1 4C-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 N^acetylation occurred prior to excretion. ------- Propham August, 1987 -5- Excretion 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 (100 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 ghort-term Exposure 0 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 LDso values in male and female rats were reported to be 3,000 ± 232 mg/kg and 2,360 ±118 mg/kg, respectively. A No-Observed-Adverse-Effect-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 m9/fcg propham (purity not 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 was 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 0 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). ------- Propham August, 1987 -6- 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 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 ?2 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 0.05 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). ------- Propham August, 1987 -7- 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. Carcinogenicity 0 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 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 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 = (NOAEL or LOAEL) x (BW) = mg/L ( ug/L) (UF) x ( L/day) ------- Propham August, 1987 -8- where: NOAEL or LOAEL = No- or Lowest-Observed-Adverse-Effect-Level in rag/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 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 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 = J50 mg/kg/day) (10 kg) , 5>0 mg/L (5,000 ug/L) (100) (1 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. 1 0 kg = assumed body weight of a child. ------- Propham August, 1987 -9- 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. The Longer-term HA for a 70-kg adult is calculated as follows: Longer-term HA = (50 mg/kg/day) (70 kg) =17.5 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 90-day study by Tisdel et al. (1979), which ------- Propham August, 1987 -10- 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) = Q.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 0 The International Agency for Research on Cancer (IARC, 1976) evaluated propham and concluded that the carcinogenic potential is indeterminate. ------- Propham August, 1987 -11- 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 carcinogenicity. VI. OTHER CRITERIA, GUIDANCE AND 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 of 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 GAC continuous- flow column. 0 The studies cited above indicate that GAC 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. ------- Propham August, 1987 -12- IX. REFERENCES Brown, J.H. and P. Gross.* 1949. Acute toxicity .study of isopropyl n-phenyl carbamate. Unpublished study. MRID 00075264. CHEMLAB. 1985. The Chemical Information System, CIS, Inc., Bethesda, MD. Chen, Y.* 1979. Summary of animal metabolism of IPC. Unpublished 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 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; 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. Unpublished 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.* 1979a. Metabolism of isopropyl carbanilate on a Woodburn silt loam soil: BR 21448. Unpublished study received Sept. 17, 1979 under 748-224; submitted by PPG Industries, Inc., Barberton, OH; CDL:240998-F. MRID 00115469. Hardies, D.E. and D.Y. Studer.* 1979b. Metabolism of isopropyl carbanilate on an Altvan loam soil: BR 21531. Unpublished 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. Unpublished 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 carbanilate on five soil types: BR 21590. Unpublished study received Sept. 17, 1979 under 748-224; submitted by PPG Industries, Inc., Barberton, OH; CDL:240987-C. MRID 00038945. ------- Propham August, 1987 -13- Hardies, D.E. and D.Y. Studer.* 1979e. A laboratory study of the leaching of isopropyl carbanilate in soils. Unpublished study prepared and submitted on Nov. 1, 1984, by PPG Industries, Inc., Chemical Division, Barberton, OH: Accession No. 255364. Hueper, W.C.* 1952. 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