820K88006 August, 198?
ENDOTHALL
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, Logrt or Probit models. There is no current
understanding of the biological mechanisms involved in cancer to suggest that
any one of these models is abne 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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Endothall
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II. GENERAL INFORMATION AND PROPERTIES
CAS No. 145-73-3
Structural Formula
COOH
7-Oxabicyclo-(2,2, 1 )-heptane-2, 3-dicarboxylic acid
Synonyms
0 1 ,2-dicarboxy3,6-endoxocyclohexane; Aquathol; Hydrothol; Des-i-cate,-
Accelerate
Uses
0 Endothall is used as a defoliant and an herbicide on both terrestrial
and aquatic weeds.
Properties (Carlson et al. , 1978; Simsiman et al. , 1976)
Chemical Formula
Molecular Weight
Physical State (25°C)
Boiling Point
Melting Point
Density
Vapor Pressure (25°C)
Specific Gravity
Water Solubility (25°C)
Log Octanol/Water Partition —
Coefficient
Taste Threshold
Odor Threshold —
Conversion Factor —
Occurrence
0 No information was found in the available literature on the occurrence
of endothall.
Environmental Fate
e No information was found in the available literature on the environ-
mental fate of endothall.
186.06
White crystalline solid
—
144°C to the anhydride
—
Negligible
— >
100 g/L (acid monohydrate)
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Endothall August, 1987
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III. PHARMACOKINETICS
Absorption
0 Few data exist regarding endothall pharmacokinetics in mammals.
Soo et al. (1967) performed pharmacokinetic experiments with male
and female Wistar rats. Approximately 82% of a 5-mg/kg oral dose
of 14c-labeled endothall (dissolved in 20% ethanol to a concentration
of 1 mg/mL) was absorbed by the rats within 72 hours. The rats had
received 5 mg/kg of unlabeled- endothall in the diet for 2 weeks prior
to treatment with 14c-endothall.
8 Deaths in rabbits directly exposed to endothall in the eye or on the
skin (Pharmacology Research, Inc, 1975a, 1975b) indicate the potential
for absorption by these routes.
Distribution
0 In the Soo et al. (1967) study, the absorbed endothall was distrib-
uted in low levels through most body tissues. Peak levels in all
tissues were observed 1 hour after dosing, with most of the dose
(about 95%) found in the stomach and intestine. Otherwise, the
tissues with the highest concentrations after 1 hour were the liver
and kidney (1.1 and 0.9% respectively), with lower concentrations
(0.02 to 0.1%) in heart, lung, spleen and brain. Very low concentra-
tions were observed in muscle, and endothall was not detected in fat.
No marked preferential accumulation was apparent.
Metabolism
0 The metabolism of endothall is not known to be characterized.
Excretion
Soo et al. (1967) described excretion as follows:
0 Clearance of 4C-endothall was biphasic in the stomach (t1 ,2 = 2-2 and
14.2 hours) and kidney (t^ » 1.6 and 34.6 hours) and monophasic
in the intestine and liver (t^ = 14.4 and 21.6 hours, respectively).
Total excretion of the 14c label was over 95% complete by 48 hours and
over 99% complete by 72 hours, suggesting that no significant
bioaccumulation occurred.
0 Approximately 90% of the administered dose was excreted in the feces.
Urinary excretion accounted fbr approximately 7% of the dose, and
approximately 3% of the radioactive label was recovered in expired
carbon dioxide.
0 Approximately 20% of the dose excreted in the feces was unchanged
endothall. The remaining radioactivity was presumed to be metabolites
or conjugates.
0 Soo et al. (1967) also found no radioactivity in pups from lactating
dams given oral doses of 14c-endothall.
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IV. HEALTH EFFECTS
Humans
0 No information was found in the available literature on the health
effects of endothall in humans except for one case history of a young
male suicide victim who ingested an estimated 7 to 8 g of disodium
endothall in solution (approximately 100 mg endothall ion/kg).
Repeated vomiting was evident. Autopsy revealed focal hemorrhages
and edema in the lungs and gross hemorrhage of the gastrointestinal
(GI) tract (Allender, 1983).
Animals
Short-term Exposure
0 Early acute studies report cardiac arrest (Goldstein, 1952) or
respiratory failure (Srensek and Woodard, 1951) as causes of death
in dogs and rabbits. Endothall was injected intravenously in both
studies with these effects observed at doses of 5 mg/kg (lowest)
and higher.
0 The available acute oral- dose studies are essentially restricted to
mortality data without biochemical or histopathological observations.
The acute toxicity of endothall acid appeared to be greater than that
of the salt forms normally used in herbicide formulations. In rats,
the oral LD50 of endothall was reported as 35 to 51 mg/kg for the
acid form and 182 to 197 mg/kg for the sodium salt (Simsiman et al.,
1976; Tweedy and Houseworth, 1976).
0 Rats were given 1,000 or 10,000 ppm disodium endothall in the diet
(Brieger, 1953a) and doses were calculated by assuming a body weight
of 0.4 kg and daily food consumption of 20 g. Slight liver degeneration
and focal hemorrhagic areas in the kidney were reported for male and
female rats dosed orally with approximately 40 mg endothall ion/kg/day
for 4 weeks; most of the rats receiving approximately 400 mg endothall
ion/kg/day died within 1 week. The liver and kidney effects from
endothall ingestion are consistent with the pharmacokinetic tissue
distribution results reported by Soo et al. (1967).
0 Nine male dogs (one dog/dose) were do-ed orally with capsules containing
1 to 50 mg disodium endothall/kg/day vO.8 to 40 mg endothall ion/kg/day)
for 6 weeks (Brieger, 1953b). All dogs that were administered 20 to
50 mg disodium endothall/kg/day died within 11 days. Vomiting and diarrhea
were observed in the group given 20 mg disodium endothall/kg/day.
Pathological changes in the GI tract, described as congested and
edematous stomach walls and edematous upper intestines, were indicated
as common in all dogs. Erosion and hemorrhages in the stomach were
observed with doses of 20 mg/kg/day or more.
Dermal/Ocular Effects
0 Goldstein (1952) reported that a 1% solution of endothall applied to
the unbroken skin of rabbits produced no effects. The same solution
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applied to scarified skin resulted in mild skin lesions. Ten to
twenty percent solutions or applications of the pure, powdered
material to intact or scarified skin resulted in more severe damage,
including necrosis, and the deaths of some treated animals.
0 Topical exposure of six rabbits to 200 mg endothall technical/kg
resulted in the death of all rabbits within 24 hours (Pharmacology
Research, Inc., 1975a).
0 Technical endothall (0.1 g equivalent to 80 mg endothall ion) produced
severe eye irritation in three rabbits when directly applied to the
conjunctiva. Effects included corneal opacity, conjunctival irritation
and iridic congestion. Furthermore, technical endothall apparently
produced systemic effects by this route of absorption, since several
animals died within 24 hours as a result of this exposure. Eyes were
rinsed with water 20 to 30 seconds after treatment in three rabbits;
conjunctival irritation and iridic congestion reversed in 4 days in
two rabbits but persisted along with corneal opacity in one rabbit
for 7 days (Pharmacology Research, Inc., 1975b).
Long-term Exposure
0 Beagle dogs (four/sex/group) fed diets containing 0, 100, 300 or
800 ppm disodium endothall (equivalent to 0, 2, 6 or 16 mg endothall
ion/kg/day for 24 months showed no gross signs of toxicity (Keller,
1965). Values for hematology, urinalysis, weight gain and food
consumption were within normal limits and comparable to those for
control animals. Increased stomach and small intestine weights were
observed in the intermediate and high-dose groups. However, microscopic
examination of essentially all tissues in the high-dose group revealed
no pathological changes that could be attributed to endothall ingestion.
A No-Observed-Adverse-Effect-Level (NOAEL) of 2 mg endothall ion/kg/day
is identified from this study.
0 Brieger (1953b) reported no toxic effects in female rats given dietary
levels as high as 2,500 ppm disodium endothall (about 100 mg endothall
ion/kg/day, assuming food intake of 20 g/day and mean body weight of
0.4 kg) for 2 years.
Reproductive Effects
0 A three-generation study in rats was reported by Scientific Associates
(1965). Groups of male and female rats were fed diets containing 0,
100, 300 or 2,500 ppm disodium endothall (equivalent to 0, 4, 12 or
100 mg endothall ion/kg/day) until they were 100 days old and were
then mated. Three successive generations of offspring were maintained
on the test diet for 100 days and then bred to produce the next test
generation. Pups in the 4-mg/kg/day dose group were normal, pups in
the 12-mg/kg/day group had decreased body weights at 21 days of age
and pups in the 100 mg/kg/day group did not survive more than 1 week.
A NOAEL for reproductive effects of 4 mg endothall ion/kg/day was
identified from this study.
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Developmental Effects
• A short-term teratology study in rats by Science Applications, Inc.
(1982) indicated no observable signs of developmental toxicity at
dose levels that were fatal to the dams. This study suggests that
the dams are. more susceptible to endothall than are the embryos or
fetuses. Groups of 25 or 26 female rats were mated and then orally
dosed with 0, 10, 20 or 30 mg/kg/day of aqueous endothall technical
(0, 8, 16 or 24 mg endothall ion/kg/day) on days 6 to 19 of gestation.
Two dams died from the 20-mg/kg/day dose, and 10 dams died from the
30-mg/kg/day dose. No clinical signs were noted prior to death, and
no lesions were observed at necropsy. The researchers concluded that
endothall technical was not embryotoxic or teratogenic at maternal
doses of 30 mg/kg/day or below. A NOAEL of 10 mg endothall
technical/kg/day based on maternal effects was identified.
Mutagenicity
0 Mutagenicity results from short-term in_ vitro tests are mixed, with
various forms of endothall reported as test agents. Mutagenicity
studies utilizing Salmonella with and without metabolic activation
resulted in negative findings for endothall technical (Andersen
et al., 1972; Microbiological Associates, 1980a). Mutagenic activity
was not found in BALB/3T3 Clone A31 mouse cells exposed to endothall
technical (Microbiological Associates, 1982b).
0 For the following studies, Wilson et al. (1956) used "commercial
Endothall" with no further description, whereas the remaining investi-
gators used Aquathol K, a commercial formulation containing dipotassium
endothall at a level of 28.6% acid equivalent. In Drosophila melano-
gaster, mutagenic results were mixed, with Wilson et al. (1956) and
Sandier and Hamilton-Byrd (1981) reporting positive and negative
results, respectively. Sandier and Hamilton-Byrd (1981) reported
negative results in a mutagenicity assay with the mold Neurospora
crassa. A sister chromatid exchange study in human lymphocytes was
negative (Vigfusson, 1981). Transformation was induced in a BALB/c
3T3 test for malignant transformation (Litton Bionetics, Inc., 1981).
Carcinogenicity
0 No statistically significant numbers or types of tumors were observed
in rats fed as much as 100 mg endothall ion/kg/day for 2 years
(Brieger, 1953b).
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
*Because the test material in the various toxicity studies was salt or acid
forms of endothall, the HAs described below are expressed in terms of
endothall ion.
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Endothall August, 1987
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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.
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 studies were located in available literature that were suitable for
calculation of the One-day HA. The single-dose studies measured mortality as
the toxicological end point and are not suitable for use in calculating an HA.
The value of 0.8 mg/L calculated as the Ten-day HA can be used as a conservative
estimate of the One-day HA.
Ten-day Health Advisory
The teratology study by Science Applications, Inc. (1982) has been
selected as the basis for the Ten-day HA. It is the only study that defined
a short-term NOAEL (8 mg endothall ion/kg/day, based on maternal toxicity).
The Ten-day HA for a 10-kg child is calculated as follows:
Ten-day HA * (a ag/kg/day) (10 kg) = 0.8 /L (800 /L)
(100) (1 L/day)
where:
8 mg/kg/day = NOAEL based on the absence of fetal and maternal
effects in rats exposed to endothall acid orally for
13 days.
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.
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Longer-term Health Advisory
There is concluded to be insufficient data for calculation of a Longer-
term HA. Therefore, the DWEL adjusted for a 10-kg child (0.2 mg/L) is propose^
as a conservative estimate for a Longer-term HA.
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 litely 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 classifed 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 riste associated with lifetime exposure to this chemical.
The 2-year feeding study in dogs by Keller (1965), which identified a
NOAEL of 2 mg endothall ion/kg/day, has been selected to serve as the basis
for the Lifetime HA for endothall. The study by Scientific Associates (1965)
was of shorter duration (100 days/generation) and did not as completely
define a NOAEL (except for 4 mg endothall ion/kg/day for reproductive effects);
however, the NOAEL in this study approximates that in the Keller (1965)
study. The 2-year study in rats by Brieger (1953b) showed no adverse effects
from doses up to 100 mg endothall ion/kg/day, but no information was provided
on the parameters tested and the levels at which effects did occur.
Using the NOAEL of 2 mg/kg/day, the Lifetime HA for endothall is calculated
as follows:
Step 1: Determination of the Reference Dose (RfD)
RfD = (2 mg/kg/day) = 0<02
where:
2 mg/Jq/day = NOAEL, based on absence of increased organ weight and
organ-body weight ratios in the stomach and small
intestine in dogs exposed to endothall in the diet
for 2 years.
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Endothall August, 1987
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100 « uncertainty factor, chosen in accordance with NAS/ODW
guidelines for use with a NOAEL from an animal study.
Step 2: Determination of the Drinking Water Equivalent Level (DWEL)
DWEL = (0.02 mg/kg/day) (70 kg) . 0>7 mg/L (700 u /L)
(2 L/day)
where:
0.02 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 * (0.7 mg/L) (20%) =0.14 mg/L (140 ug/L)
where:
0.7 mg/L » DWEL.
20% » assumed percentage of daily exposure contributed by
ingestion of drinking water.
Evaluation of Carcinogenic Potential
0 Available toxicity data do not show endothall as carcinogenic.
0 Endothall can be placed in Group D (inadequate evidence in humans
and animals) by the EPA's guidelines for carcinogenic risk assessment
(U.S. EPA, 1986).
8 The International Agency for Research on Cancer has not evaluated the
carcinogenic potential of endothall (WHO, 1982).
VI. OTHER CRITERIA, GUIDANCE AND STANDARDS
8 An interim tolerance of 200 ug/L has been published for residues of
endothall, used to control aquatic plants, in potable water (CFR,
1979).
8 Residue tolerances for endothall published by the U.S. EPA (CFR,
1977) include 0.1 ppm in or on cottonseed, 0.1 ppm in or on potatoes,
0.05 ppm in or on rice grain and 0.05 ppm in or on rice straw.
0 A tolerance is a derived value based on residue levels, toxicity
data, food consumption levels, hazard evaluation and scientific
judgment; 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).
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0 The ADI set by the U.S. EPA Office of Pesticide Programs is 0.02
rag/kg/day based on the 2 mg/kg/day NOAEL in the 2-year dog study by
Keller (1965) and a 100-fold uncertainty factor.
VII. ANALYTICAL METHODS
0 No information was found in the available literature on the analytical
methods used to detect endothall in drinking water.
VIII. TREATMENT TECHNOLOGIES
8 No information was found in the available literature on treatment
technologies capable of effectively removing endothall from contaminated
water.
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Endothall August, 1987
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IX. REFERENCES
Allender, W.J. 1983. Suicidal poisoning by endothall. J. Anal. Toxicol.
7:79-82.
Andersen, K.J., E.G.-Leighty and M.T. Takahashi. 1972. ^Evaluation of herbi-
cides for possible mutagenic properties. J. Agr. Food Chem. 20:649-654.
Brieger, H.* 1953a. Preliminary studies on the toxicity of endothall
(disodium). EPA Pesticide Petition No. 6G0503, redesignated No. 7F0570,
1966. Accession No. 246012.
Brieger, H.* 1953b. Endothall, long term oral toxicity test—rats. EPA
Pesticide Petition No. 6G0503, redesignated No. 7F0570, 1966. Accession
No. 246012.
Carlson, R., R. Whitaker and A. Landskov. 1978. Endothall. Chapter 31.
In G. Zweig and J. Sherma, eds. Analytical methods for pesticides and
plant growth. New York: Academic Press, pp. 327-340.
CFR. 1977. Code of Federal Regulations. 40 CFR 180.293.
CFR. 1979. Code of Federal Regulations. 21 CFR 193.180. April 1, 1979.
Goldstein, F. 1952. Cutaneous and intravenous toxicity of endothall
(disodium-3-endohexahydrophthalic acid). Pharmacol. Exp. Ther. 11:349.
Keller, J.* 1965. Two year chronic feeding study of disodium endothall to
beagle dogs. Scientific Associates report. EPA Pesticide Petition
6G0503, redesignated No. 7F0570, June 1966. Accession No. 24601.
Litton Bionetics, Inc. 1981. Evaluation of Aquathol K in the in vitro
transformation of BALB/3T3 cells with and without metabolic activation
assay. Project No. 20992. Report to Municipality of Metropolitan
Seattle, Seattle, WA, by Litton Bionetics, Inc., Rockville, MD.
Microbiological Associates.* 1980a. Activity of T1604 in the Salmonella/
microsomal assay for bacterial mutagenicity. Unpublished final report
for Pennwalt Corp. by Microbiological Associates, Bethesda, MD.
Microbiological Associates.* 1980b. Activity of T1604 in the in vitro
mammalian cell point mutation assay in the absence of exogenous metabolic
activation. Unpublished final report for Pennwalt Corp. by Microbiological
Associates, Bethesda, MD.
Paynter, O.E., J.G. Cummings and M.H. Rogoff. Undated. United States
Pesticide Tolerance System, U.S. EPA, Office of Pesticide Programs,
Washington, DC. Unpublished draft report.
Pharmacology Research, Inc.* 1975a. U.S. EPA Pesticide Resubmission File
4581-EIE. Summary data on acute oral toxicity and dermal irritation in
rabbits (Endothall). Accession No. 244125.
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Endothall August, 1987
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Pharmacology Research, Inc.* 1975b. U.S. EPA Pesticide Resubmission File.
Summary data, primary eye irritation in the rabbit and inhalation toxicity
in several species (Endothall). Accession No. 246012.
Sandier, L., and E.L. Hamilton-Byrd. 1981. The induction of sex-linked
recessive ethal mutations in Drosophila melanogaster by Aquathol K, as
measured by the Muller-5 test. Report to Municipality of Metropolitan
Seattle, Seattle, WA.
Scientific Associates.* 1965. Three generation rat reproductive study,
disodium endothall. EPA Pesticide Petition No. 6G0503, redesignated
7F0570, 1966. EPA Accession No. 114667.
Science Applications, Inc.* 1982. A dose range-finding teratology study of
endothall technical and disodium endothall in albino rats. Resubmission
of Pesticide Application for Aquathol K Aquatic Herbicide (EPA Registra-
tion No. 4581-204) and Hydrothal 191 Aquatic Algicide and Herbicide
(EPA Registration No. 4581-174). EPA Accession No. 071249.
Simsiman, G.V., T.C. Daniel and G. Chesters. 1976. Diquat and endothall:
Their fates in the environment. Res. Rev. 62:131-174.
Soo, A., I. Tinsley and S.C. Fang. 1967. Metabolism of 14C-endothall in
rats. J. Agric. Food Chem. 15:1018-1021.
Srensek, S.E., and G. Woodard. 1951. Pharmacological actions of "endothall"
(disodium-3,6-endoxo-hexahydrophthalic acid). Fed. Proc. 10:337.
(Abstract)
Tweedy, B.C., and L.D. Houseworth. 1976. Miscellaneous herbicides. In
Herbicides-chemistry, degradation and mode of action. P.C. Kearney and
D.D. Kaufman, eds. Chapter 17. New York: Marcel Dekker, Inc., pp.
815-833.
U.S. EPA. 1986. U.S. Environmental Protection Agency. Guidelines for
carcinogen risk assessment. Fed. Reg. 51(185) :33992-34003.
September 24.
Vig'fusson, N.V. 1981. Evaluation of the mutagenic potential of Aquathol K
by induction of sister chromatid exchanges in human lymphocytes in vitro.
Report to Municipality of Metropolitan Seattle, Seattle, WA.
WHO. 1982. World Health Organization. IARC monographs on the evaluation of
the carcinogenic risk of chemicals to humans. Chemicals, industry
processes and industries associated with cancer to humans. International
Agency for Research on Cancer Monographs Vol. 1 to 29. Supplement 4.
Geneva: World Health Organization.
Wilson, S.M., A. Daniel and G.B. Wilson. 1956. Cytological and genetical
effects of the defoliant endothall. J. Hered. 47:151-154."
Confidential Business Information submitted to the Office of Pesticide
Programs.
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