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.
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Butylate
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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.
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Butylate August, 1987
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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.
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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
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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).
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• 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
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Butylate August, 1987
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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.
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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.
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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
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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)
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Butylate August, 1987
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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.
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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.
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Butylate August, 1987
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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
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