August, 1987 820K88124 BUTYLATE Health Advisory Office of Drinking Water U.S. Environmental Protection Agency DRAFT 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. ------- Butylate August, 1987 -2- II. GENERAL INFORMATION AND PROPERTIES CAS No. 2008-41-5 Structural Formula H5c2-s-c-N; \. •CH2CH(CH3)2 Carbamothioic acid, bis(2-methylpropyl)-, S-ethyl ester Synonyms S-ethyl di-isobutylthiocarbamate; S-ethyl bis(2-methylpropyl) carbamothioate; ethyl N,N-di-isobutyl thiocarbamate; S-ethyl-di-isobutyl thiocarbamate; ethyl-N,N-di-isobutyl thiolcarbamate; R-1910; Sutan*. Uses • ° Selective preplant herbicide (Meister, 1983). Properties (BCPC, 1977) Chemical Formula Molecular Weight Physical State (25°C) Boiling Point Melting Point Density (25°C) Vapor Pressure (258C) Specific Gravity Water Solubility (20eC) Octanol/Water Partition Coefficient Taste Threshold Odor Threshold Conversion Factor CnH23NOS 217.41 Clear liquid, aromatic odor 138°C 0.9417 1.3 x 10-3 nun Hg 45 rag/L Occurrence Butylate has been found in 298 of 431 surface water samples analyzed and in none of 18 ground water samples (STORET, 1987). Samples were collected at 52 surface water locations and 18 ground water locations, and butylate was found in 5 states. The 85th percentile of all nonzero samples was 0.17 ug/L in surface water and 0 ug/L in ground water sources. The maximum concentration found was 6 ug/L in surface water and in 0 ug/L in ground water. ------- Butylate August, 1987 -3- Environmental Fate 0 Butylate degrades fairly rapidly in moist soils under aerobic condi- tions; half-lives were 3 to 10 weeks (Thomas and Holt, 1979; Shell Development Company, 1975; Stauffer Chemical Company, 1975a). Under anaerobic conditions, butylate degrades with a half-life of 13 weeks (Thomas et al., 1978). Butylate sulfoxide is the major degradate, but s-ethyl-2,2-dimethyl-2-hydroxyethylisobutyl thiocarbamate, diisobutylformamide, diisobutylamine, diisobutylthiocarbamate, and isobutylamine were also identified as degradates (Thomas and Holt, 1979; Thomas et al., 1978; Shell Development Company, 1975; Stauffer Chemical Company, 1975a). 0 Butylate is slightly mobile to highly mobile in soils ranging in texture from silty clay loam to gravelly sand (Gray and Weierich, 1966; Lavy, 1974; Thomas and Holt, 1979; Weidner, 1974). 0 Butylate is fairly volatile; 45 to 50% of 14C- butylate applied to moist (20% moisture) Sorrento clay loam was recovered as volatile radioactivity over 3 weeks following treatment. Volatile radioactivity was characterized as butylate (Thomas and Holt, 1979). 0 In the field, butylate dissipated more readily in a soil in Florida than in a silty clay loam in California, probably leaching beyond the 6-inch sampling depth. The estimated half-lives in the upper 6 inches of the sand were 28 and 18 days when a 4 Ib/gal Mcap and a 6.7 Ib/gal EC formulation, respectively, were applied at 8 Ib ai/A. For the silty clay loam, estimated half-lives were more than 64 days for both the Mcap and a 7 Ib/gal EC formulation applied at 8 Ib ai/A (active ingredient/acre) (Stauffer Chemical Company, 1975b; Stauffer Chemical Company, 1975c). 0 Butylate has a low bioaccumulation potential in bluegill sunfish. A bioconcentration factor of 33 was found in the edible portion of fish dosed with !4C-butylate at 0.01 or 1 ppm for 28 days. The nonedible portion of fish dosed at 0.01 and 1 ppm exhibited bioconcentration factors of 174 and 122, respectively. After 10 days of depuration, 50 to 67% of the day-28 residues was lost (Sleight, 1973). III. PHARMACOKINETICS Absorption 0 Data relating specifically to the absorption of butylate were not located in the available literature; however, some information was obtained from a metabolism study by Hubbell and Casida (1977). Doses of 12.3 or 156.0 mg/kg 14co-labeled butylate were administered by gavage to male albino Sprague-Dawley rats weighing 190 to 210 g. Within 48 hours, 27.3 and 31.5% of the administered radioactivity were recovered in the urine, and 60.9 and 64.0% were expired as 14C02 in the low- and high-dose groups, respectively. These results indicate that butylate is appreciably absorbed from the gastrointestinal tract of rats. ------- Butylate August, 1987 Distribution • Hubbell and Casida (1977) measured the tissue radioactivity 48 hours after the administration by gavage of 12.3 or 156.0 mg 14co-labeled butylate/kg to male Spr ague-Da wley rats. At the low dose, 2.4% of the administered radioactivity was retained in the body, with levels of radioactivity equivalent to 276 ppb in the blood, 524 ppb in the kidney, 710 ppb in the liver and a range of 182 to 545 ppb in other tissues (brain, fat, heart, lung, muscle, spleen and testes). At the high dose, 2.2% of the radioactivity was retained in the body with 2,076 ppb in the blood, 5,320 ppb in the kidney, 7,720 ppb in the liver and 1,720 to 5,560 ppb in other tissues. Metabolism 0 Hubbell and Casida (1977) followed the metabolism of butylate in male Spr ague-Da wley rats based upon identification of the 48-hour urinary metabolites of 14CO- labeled preparations of butylate (12.3 or 156 n9/kg). Degradation of administered butylate metabolites was also assessed. Approximately 40% of the administered 14co-butylate was metabolized by ester cleavage and 4C02 liberation without going through the sulf oxide (the major metabolite) as an intermediate. The metabolites from all compounds were essentially the same qualitatively and quantitatively. The metabolites for 14CO-butylate included, as percent of urinary radioactivity, 4.3% as the N,N-di-isobutyl mercapturil acid, 17.1% as the N-isobutylmercapturic acid, 0.8% as the mercaptoacetic" acid derivative, 11.7% as the glycine conjugate of the mercaptoacetic acid derivative and about 66% as at least 15 other metabolites. 0 S-(1-14c)ethyl-Sutan®, orally administered at about 110 mg Sutan*/kg» was readily degraded and excreted by male and female Sprague-Dawley rats (Thomas et al., 1980). Cleavage of the S-ethyl moiety and the incorporation of the two-carbon fragment into intermediary metabolic pathways accounted for >70% of the total administered radiocarbon. Urinary excretion of 14C-hippuric acid, ethyl methyl sulf oxide and ethyl methyl sulfone was evident. Excretion Hubbell and Casida (1977) administered 12.3 or 156 mg/kg of 1 Re- labeled butylate by gavage to adult male Sprague-Dawley rats. Withi-r 24 hours, 60.9 and 64.0% of the administered radioactivity were expired as CC>2, 27.3 and 31.5% were excreted in the urine and 3.3 and 4.7% were excreted in the feces in the low- and high-dose groups, respectively. A study by Bova et al. (1978) indicates that biotransformation of S-(1-14c) ethyl-Sutan* in male and female Sprague-Dawley rats given oral doses of 83.5 to 133.5 mg Sutan*/kg involves rapid cleavage of the S-ethyl moiety. Degradation of this fragment of the molecule results in the release of 14C02 as the major product of metabolism, accounting for 69% of the total administered dose. This rapid pro- duction of 14C02 may account for the relatively high levels (7.8%) of ------- Butylate . August, 1987 found in the tissues after 8 days. Urine and feces accounted for 13.9 and 3.2% of the 1 4c dose, respectively. Data obtained from a 3-day balance and tissue residue study by Thomas et al. (1979) show that (1-14c-isobutyl)Sutan* is readily eliminated by male and female Sprague-Dawley rats after a single oral dose (about 100 mg Sutan*/kg). More than 99% of the administered radiocarbon was recovered from the animals within 72 hours after dosing. Most of the dose (94%) was recovered within 24 hours after treatment. Less than 0.5% of the radiocarbon remained in the tissues after 72 hours, and the Sutan® equivalents in organ and tissue samples were all less than 2 ppm. Urine, feces and expired 14C02 accounted for 93.7, 4.0 and 2.0% of the dose, respectively. IV. HEALTH EFFECTS Humans No information was found in the available literature on the health effects of butylate in humans. Animals Short-term Exposure 0 The acute oral LD5g value in male and female rats given butylate technical (85.71% pure) was 3.34 and 3.0 g/kg, respectively (Raltech, 1979). Dermal/Ocular Effects 0 Skin irritation was observed in rabbits topically exposed to 2 g butylate technical (85.71% pure) for 24 hours (Raltech, 1979). 0 Topical application of R-1910 6E technical (97.5% pure) at doses of 20 and 40 mg active ingredient (a.i.)/kg, 5 days per week for a total of 21 applications, was without observed effect except for local skin irritation (Woodard Research Corp., 1967a). 0 Application of butylate technical (85.71% pure) to the eyes of rabbits resulted in irritation and corneal opacity. No corneal opacity was in eyes washed after treatment (Raltech, 1979). Long-term Exposure 0 Dietary feeding of R-1910 technical (97.5% pure) to male and female Charles River rats at dose levels of 32, 16 and 8 mg/kg/day for 13 weeks was without observable adverse effect. The high dose (32 mg/kg/day) was identified as the No-Observed-Adverse-Effect-Level (NOAEL) for this study (Woodard Research Corp., 1967b). ------- Butylate August, 1987 « -6- • Dietary feeding of Sutan* Technical and Sutan* Analytical (purities not specified) to male Sprague-Oawley rats at dose levels as high as 180 mg/kg/day for 15 weeks was without observable adverse effect (NOAEL) (Scholler, 1976). 0 Results of a toxicity study in which male and female beagle dogs were fed R-1910 Technical (97.6% pure) at dietary levels of 450, 900 and 1,800 ppm (corresponding to doses of 11, 23 and 45 mg/kg/day, assuming 1 ppm equals 0.025 mg/kg/day from Lehman, 1959) for 16 weeks were unremarkable (Woodard Research Corp., 1967c). Hence, 45 mg/kg/day is identified as a NOAEL. 0 Sutan* Technical (98% pure) was fed in the diet to male and female Sprague-Dawley rats at dose levels of 10, 30 and 90 mg/kg/day for 56 weeks. One group of rats was given 90 mg/kg/day for 15 weeks followed by 180 mg/kg/day for 41 weeks. No systemic effects were found at 10 mg/kg/day (NOAEL). Testes/body weight ratios were significantly (p <0.05) lower in terminally sacrificed males given 30 and 90 mg/kg/day. Slight (8 to 15%) nonsignificant (p >0.05) mean body weight decreases were found in 30 and 90 nsg/kg males and 90 mg/kg females. Liver to body weight increases and testicular lesions were found with the highest doses. Blood clotting parameters were affected at all doses, with the effects at 10 mg/kg/day being significant (p <0.05) decreases in factor II times in males and activated partial thromboplastin times in females (Hazelton Laboratories, Inc., 1978). 0 R-1910 Technical (purity not specified) was fed in the diet to male and female Sprague-Oawley CD rats at dose levels of 50, 100, 200 and 400 mg/kg/day for 2 years. Although significantly (p <0.05) elevated liver-to-body weight ratios occurred in terminally sacrificed males given 50 mg/kg/day, this effect was not observed in animals from this dose group sacrificed at 12 and 18 months. Hence, 50 mg/kg/day was identified as a NOAEL. In males and females, body weights were significantly (p <0.05) reduced, and liver to body weight ratios were significantly (p <0.05) increased with doses above 50 mg/kg/day. Neoplastic nodules and periportal hypertrophy in the liver were significantly (p <0.05) increased in males given 400 mg/kg/day (Biodynamics, 1982). 0 Male and female Charles River CD-I mice were given Sutan* Technical (98% pure) in the diet at dose levels of 20, 80 and 120 mg/kg/day for 2 years. No effects were found at 20 mg/kg/day (NOAEL). Kidney and liver lesions were noted with higher doses (International Research and Development Corporation [IRDC], 1979). Reproductive Effects 0 No information was found in the available literature on the effects of butylate on reproduction. Developmental Effects • Sutan* Technical (98.2% pure) was administered by gavage to pregnant rats at doses of 40, 400 and 1,000 mg/kg/day on days 6 through 20 of ------- Butylate August, 1987 -7- gestation. The 40 mg/kg/day dose was without observable effect (NOAELK Higher doses decreased body weight gain in dams, increased liver-to- body weights in dams, decreased fetal body weights, increased incidences of misaligned sternebrae and delayed ossification, and increased early resorptions. Sutan® was not teratogenic in this study (Stauffer Chemical Co., 1983). 0 Administration of R-1910 Technical (97.6% pure) in the diet to pregnant Charles River mice at dose levels of 4, 8 and 24 mg/kg/day either on days 6 through 18 or from day 6 until natural delivery was without observable effect (NOAEL) on dams and fetuses (Woodard Research Corp., 1967d). Mutagenicity 0 Butylate was not mutagenic in Salmonella typhimurium strains TA1535, TA1537, TA1538 and TA100 with or without the S-9 activating fraction (Eisenbeis et al., 1981). 0 in Drosophila melanogaster, butylate treatment increased the frequency of sex-linked recessive lethals but had no effect on the frequency of dominant lethals (Murnik, 1976). Carcinogenicity 0 R-1910 Technical was not determined to be carcinogenic in the 2-year rat study by Biodynamics (1982), but a significant (p <0.05) increase in neoplastic nodules in liver in high-dose males was evident. Neoplastic nodules were found in 2/69, 6/69, 1/69, 1/70 and 9/70 males given 0 ppm (control), 50 ppm, 100 ppm, 200 ppm and 400 ppm, respectively. Hepatocellular carcinomas were found in 2/69, 3/69, 4/69, 3/70 and 2/70 males given 0 ppm (control), 50 ppm, 100 ppm, 200 ppm and 400 ppm, respectively. 0 Sutan® Technical was not carcinogenic in the 2-year mouse study by IRDC (1979). 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) where: NOAEL or LOAEL = No- or Lowest-Observed-Adverse-Effect-Level in mg/kg bw/day. ------- Butylate August, 1987 -8- 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 butylate. It is, therefore, recommended that the Ten-day HA value (2.4 mg/L, calculated below) be used at this time as a conservative estimate of the One-day HA value. Ten-day Health Advisory The teratology study in mice by Woodard Research Corporation (1967d) has been selected to serve as the basis for determination of the Ten-day HA value for butylate because it provides a short-term NOAEL (24 mg/kg/day for 13 days) for both maternal and fetal toxicity. The teratology study in rats by Stauffer (1983), which identified a NOAEL of 40 mg/kg/day (for 15 days) for maternal and fetal effects, could also be considered; however, because doses higher than the 24 mg/kg/day NOAEL were not included in the Woodard study (1967d), the effect levels in this study are uncertain. Furthermore, the agent was given in the diet in the Woodard study (1967d) and by gavage in the Stauffer (1983) study. Therefore, dose-response comparisons in terms of both effect and no-effect levels between the Woodard (1967d) and Stauffer (1983) studies cannot be made. Using a NOAEL of 24 mg/kg/day, the Ten-day HA for a 10-kg child is calculated as follows: Ten-Day HA = (24 mg/kg/day) (10 kg) = 2.4 mg/L (2,400 ug/L) (1 L/day) (100) where: 24 mg/kg/day = NOAEL based on the absence of fetal and maternal effects in mice exposed to Sutan* Technical orally for 13 days. 10 kg = assumed body weight of a child. 1 L/day = assumed daily water consumption of a child. 100 * uncertainty factor, chosen in accordance with National Academy of Sciences/Office of Drinking Water (NAS/ODW) guidelines for use with a NOAEL from an animal study. ------- Butylate August, 1987 -9- Longer-term Health Advisory The DWEL (2.45 mg/L) is recommended for use as a conservative estimate of the Longer-term HA by the rationale given below. The 56-week feeding study with Sutan® Technical in rats by Hazelton Laboratories (1978) is a possible basis for a Longer-term HA. However, effects observed in this study were not evident with higher doses in the 2-year feeding study with R-1910 Technical in rats by Biodynamics, Inc. (1982). The 20 mg/kg/day NOAEL in the 2-year mouse study by the International Research and Development Corporation (IRDC) (1979) used to calculate the Lifetime HA is concluded to be consistent with the data in the 56-week study by Hazelton (1978) in that it is between the 30 mg/kg/day dose, where the observed effect was decreased testes/body weight ratios, and the 10 mg/kg/day NOAEL in the latter study. Effects on blood clotting parameters (decrease in factor II times in males and activated partial thromboplastin times in females) at the 10 mg/kg/day dose and higher in the Hazelton (1978) study are considered to be of questionable toxicological significance because it is not certain whether they actually represent adverse effects, and these effects were not found in the 2-year rat study by Biodynamics (1982). The 16-week and 13-week feeding studies with R-1910 Technical in dogs and rats, respectively, by Woodard Research Corp. (1967b,c) can also be proposed for calculation of the Longer-term HA. However, the highest estimated dose of 45 mg/kg/day was the NOAEL in the dog study, and the highest dose of 32 mg/kg/day was the NOAEL in the rat study. These NOAELs are also higher than the 30 mg/kg/day dose where testicular effects were evident in the Hazelton (1978) study in rats, though these effects are overshadowed by the failure to repeat them in the 2-year rat study by Biodynamics (1982), and use of doses between the 20 mg/kg/day NOAEL and the 80 mg/kg/day LOAEL in the IRDC (1979) mouse study could have provided a closer comparison of dose-response across species. Consequently, the 20 mg/kg/day NOAEL in the mouse study by IRDC (1979) is concluded to be an effective NOAEL across species used in presently available butylate toxicity studies. 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 ------- Butylate August, 1987 -10- 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. EPAa, 1986), then caution should be exercised in assessing the risks associated with lifetime exposure to this chemical. The 2-year feeding study on Sutan® Technical in mice by IRDC (1979) has been selected to serve as the basis for the Lifetime HA value for butylate. Although the NOAEL of 20 mg/kg/day is lower than the NOAEL of 50 mg/kg/day in the 2-year feeding study with Sutan® Technical in rats by Biodynamics (1982), the mouse study is used, following the reasons given under the Longer-term HA. The Lifetime HA is calculated as follows: Step 1: Determination of the Reference Dose (RfD) RfD - (20 mg/kg/day) _ 0.07 mg/kg/day (70 ug/kg/day) (100) (3) where: 20 mg/kg/day = NOAEL, based on the absence of toxic signs in mice exposed to butylate in the diet for 2 years.. 100 = uncertainty factor, chosen in accordance with NAS/ODW guidelines for use with a NOAEL from an animal study. 3 = additional uncertainty factor used by EPA/Office of Pesticide Programs to account for the absence of major studies (chronic feeding in dogs, reproduction in rats, teratology in rabbits) which does not make it possible to establish the most sensitive end point for butylate. Step 2: Determination of the Drinking Water Equivalent Level (DWEL) DWEL = (0.07 mg/kg/day) (70 kg) = 2.45 mg/L (2,450 ug/L) (2 L/day) where: 0.07 mg/kg/day = RfD. 70 kg = assumed body weight of adult. 2 L/day = assumed daily water consumption of an adult. Step 3: Determination of the Lifetime Health Advisory Lifetime HA - (2.45 mg/L)(20%) „ 0<05 mg/L (50 ug/L) ------- Butylate August, 1987 -11- where: 2.45 mg/L - DWEL. 20% = assumed relative source contribution from water. 10 = uncertainty factor, chosen in accordance with Office of Drinking Water (ODW) policy for use with Group C carcinogens. Evaluation of Carcinogenic Potential 0 Available toxicity data do not determine butylate to be carcinogenic, although a significant (p <0.05) increase in neoplastic nodules in the liver of male rats fed the highest dose in the 2-year study by Biodynamics (1982) was found. 0 Applying the criteria described in EPA's guidelines for assessment of carcinogenic risk (U.S. EPA, 1986a), butylate may be placed in Group C: a possible human carcinogen. This category is for substances that show limited evidence of carcinogenicity in animals and inadequate evidence in humans. 0 The U.S. EPA has not calculated excess lifetime cancer risks for this material. VI. OTHER CRITERIA, GUIDANCE AND STANDARDS 0 Residue tolerances for butylate have been established by the U.S. EPA (1985) and include 0.1 ppm in or on corn grain, fresh corn, corn forage and fodder, sweet corn and popcorn. A tolerance is a derived value based on residue levels, toxicity data, food consumption levels, hazard evaluation and scientific judgment, and it is the legal maximum concentration of a pesticide in or on a raw agricultural commodity or other human or animal food (Paynter et al., undated). 0 The U.S. EPA Office of Pesticide Programs has calculated a provisional ADI of 70 ug/kg/day, based on the 20-mg/kg/day NOAEL in the 2-year mouse study by IRDC (1979) and a 300-fold uncertainty factor (used because of data gaps, including a chronic feeding study in dogs, a reproduction study in rats and a teratology study in rabbits, in the total data package). VII. ANALYTICAL METHODS * Analysis of butylate is by a gas chromatographic (GC) method applicable to the determination of certain nitrogen- and phosphorus-containing pesticides in water samples -(U.S. EPA, 1986b). In this method, approximately 1 L of sample is extracted with methylene chloride. The extract is concentrated and the compounds are separated using capillary column GC. Measurement is made using a nitrogen-phosphorus detector. ------- Butylate August, 1 987 -12- The method detection limit has not been determined for butylate, but it is estimated that the detection limits for analytes included in this method are in the range of 0.1 to 2 ug/L. VIII. TREATMENT TECHNOLOGIES 0 No information was found in the available literature on treatment technologies capable of effectively removing butylate from contaminated water. ------- Butylate August, 1987 -13- IX. REFERENCES BCPC. 1977. British Crop Protection Council. Pesticide Manual, 5th ed. Nottingham, England: Boots Company, Ltd., p. 5S3. Biodynamics, Inc.* 1982. A two-year oral toxicity/carcinogenicity study of R-1910 in rats. Project no. 78-2169. Submitted to Stauffer Chemical Co., Richmond, CA. Unpublished final report. MRID 00125678. Bova, D.L., J.R. DeBaun, J.C. Petersen and J.J. Menn. 1978.* Metabolism of [ethyl-14c] Sutan in the rat: Balance and tissue residue. Stauffer Chemical Co., Richmond, CA. Unpublished final report. MRID 00043681. Casida, J.E., R.A. Gray and H. Tilles. 1974. Thiocarbamate sulfoxides. Potent, selective and biodegradable herbicides. Science. 184:573-574. Eisenbeis, S.J., D.L. Lynch and A.E. Hampel. 1981. The Ames mutagen assay tested against herbicides and herbicide combinations. Soil Sci. 131 (1):44-47. Gray, R.A., and A.J. Weierich.* 1966. Behavior and persistence of S-ethyl- diisobutylthiocarbamate (Sutan) in soils. Unpublished study. Stauffer Chemical Company, Richmond, CA. Hazelton Laboratories America, Inc.* 1978. Fifty-six-week feeding study in rats. Sutan Technical. Project no. 132-135. Submitted to Stauffer Chemical Co., Richmond, CA. Unpublished final report. MRID 00035843. Hubbell, J.P., and J.E. Casida. 1977. Metabolic fate of the N,N'-dialkyl- carbamoyl moiety of thiocarbamate herbicides in rats and corn. J. Agric. Food Chem. 25(2):404-413. IRDC.* 1979. International Research and Development Corporation. Sutan Technical. Lifetime oral study in mice. Submitted to Stauffer Chemical Co., Richmond, CA. Unpublished final report. MRID 00035844. Lavy, T.L. 1974. Mobility and deactivation of herbicides in soil-water systems: Project A-024-NEB, University of Nebraska, Water Resources Research Institute. Submitted by Shell Chemical Company, Washington DC. Available from National Technical Information Service (NTIS), Springfield, VA; PB-238-632. Lehman, A. J. 1959. Appraisal of the safety of chemicals in foods, drugs and cosmetics. Association of Food and Drug Officials of the United States. Meister, R., ed. 1983. Farm chemicals handbook. Willoughby, OH: Meister Publishing Company. Murnik, M.R. 1976. Mutagenicity of widely used herbicides. Genetics. 83:554. Paynter, O.E., J.G. Cummings and M.H. Rogoff. Undated. United States Pesticide Tolerance System. U.S. EPA, Office of Pesticide Programs. Unpublished draft report. ------- Butylate August, 1987 -14- Raltech.* 1979. Project nos. 74489 and 733422. Submitted to Stauffer Chemice) Co., Richmond, CA. Unpublished final report. Scholler, J.* 1976. Fifteen-week oral (diet) toxicity study with Sutan Technical and Analytical in male rats: Experiment 7. Unpublished final report. MRID 00021844. Shell Development Company.* 1975. Dissipation of Bladex herbicide and Sutan in soil following application of Bladex, Sutan, or a tank mix of Bladen and Sutan: TIR-24-134-74. Unpublished study. Sleight, B.H., ill.* 1973. Exposure of fish to He-labeled Sutan: Accumulation, distribution, and elimination of 14c residues. Unpublished study prepared by Bionomics, Inc., submitted by Stauffer Chemical Company, Richmond, CA. Stauffer Chemical Company.* 1975a. Dissipation of Bladex herbicide and Sutan in soil following application of Bladex, Sutan, or a tank mix of Bladex and Sutan: TIR-24-134-74. Unpublished study submitted by Stauffer Chemical Company, Richmond, CA. Stauffer Chemical Company.* 1975b. Residues from Sutan on soil: FSDS Nos. A-9229, A-9229-1, A-9229-2, A-10366. Unpublished study by Stauffer Chemical Company, Richmond, CA. Stauffer Chemical Company.* 1975c. Soil residue data of Sutan combinations and R-25788: FSDS Nos. A-9229, A-9229-1, A-9229-2, A-10366. Unpublished study by Stauffer Chemical Company, Richmond, CA. Stauffer Chemical Company.* 1983. A teratology study in CD rats with Sutan Technical. Project no. T-11713. Unpublished final report by Stauffer Chemical Company, Richmond, CA. MRID 000131032. STORET. 1987. Thomas, D.B., J.B. Miaullis, A.R. Vispetto and J. Osuna.* 1979. Metabolism of [isobutyl-14C] Sutan in the rat: Balance and tissue residue study. Stauffer Chemical Co., Richmond, CA. Unpublished final report. MRID 00043680. Thomas, D.LtB., J.C. Petersen and J.R. DeB=iun.* 1980. Metabolism of [1-14C-ethyl] Sutan in the rat: Urinary metabolite identification. Stauffer Chemical Co., Richmond, CA. Unpublished final report. MRID 00043682. Thomas, V.M., and C.L. Holt.* 1979. Behavior of Sutan in the environment: MRC-B-76; MRC-78-02. Unpublished study submitted by Stauffer Chemical Company, Richmond, CA. Thomas, V.M., C.L. Holt and P.A. Bussi.* 1978. Anaerobic soil metabolism of Sutan selective herbicide: MRC-B-98; MRC-79-13. Unpublished study submitted by Stauffer Chemical Comapny, Richmond, CA. ------- Butylate August, 1987 -15- U.s. EPA. 1985. U.S. Environmental Protection Agency. Residue tolerances for S-ethyl-diisobutyl thiocarbamate. CFR 180.232. July 1. p. 294. U.S. EPA. 1986a. U.S. Environmental Protection Agency. 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