United States Office of Prevention, Pesticides
Environmental Protection and Toxic Substances
Agency (7501C)
PESTICIDE FACT SHEET
Name of Chemical: DIMETHOMORPH
Reason for Issuance: New Pesticide Registration
Date Issued: September 30,1998
DESCRIPTION OF CHEMICAL
Generic Name: (E,Z) 4-[3-(4-chlorophenyl)-3-(3,4-dimethoxyphenyl)-l-oxo-2-
propenyljmorpholine
Common Name: Dimethomorph
Trade Names/EPA Reg. Nos.: Acrobat® Fungicide Technical/241 -382
Acrobat® MZ Fungicide/241-383
Acrobat® WDG Fungicide/241-395
EPA Chemical Code: 268800
Chemical Abstracts Service (CAS) No: 110488-70-5
Year of Initial Registration: 1998
Pesticide Type: Systemic Morpholine Fungicide
U.S. Producer: American Cyanamid Company
USE PATTERNS AND FORMULATIONS
Application Sites: Dimethomorph is a systemic morpholine fungicide for use on potatoes. Its
mode of action is the inhibition of sterol (ergosterol) synthesis. Morpholines are all systemic
with curative and preventative qualities. Dimethomorph was developed for downy mildews, late
blights, crown and root rots for grapes, potatoes, tomatoes, and other vegetables. Time-limited
tolerances (in conjunction with Section 18 requests) are also established under 40 CFR §180.493
for residues of the fungicide dimethomorph in or on various raw agricultural commodities
(RAC's) including cantaloupes, cucumbers, potatoes, squash, tomatoes, and watermelons.
Formulation Types:
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98.98% dimethomorph Solid powder
9.00% dimethomorph + 60% mancozeb Water-dispersible granules
9.00% dimethomorph + 60% mancozeb Wettable powder
Application Types and Methods: Ground and aerial application and through sprinkler
irrigation systems (center-pivot, lateral move, side (wheel) roll and solid set), or hand-move
irrigation systems.
Application Rates: A maximum of five applications at a rate of 2.25 Ib. per acre of formulated
product (0.2 Ib. dimethomorph active ingredient per acre) per season.
Carrier: Water
SCIENCE FINDINGS
Summary Science Statements
A tolerance is established for residues of the fungicide dimethomorph [(E,Z) 4-[3-(4-
chlorophenyl)-3-(3,4-dimethoxyphenyl)-l-oxo-2-propenyl]morpholine] in or on potatoes at 0.05
ppm and potatoes, wet peel at 0.25 ppm. Based upon a battery of acute toxicity studies,
dimethomorph technical is relatively non-toxic when administered acutely to laboratory animals
and is classified as Toxicity Category III. EPA determined a reference dose (RfD) of 0.1
mg/kg/day based on the NOAEL of 11 mg/kg/day from the rat oncogenicity study and was
supported by similar results in the rat chronic dietary study in which there were significant body
weight decrement and liver effects in female rats at the LOAEL of 46.3 mg/kg/day. An
uncertainty factor (UF) of 100 which was applied to account for both the interspecies
extrapolation and the intraspecies variability. EPA has classified dimethomorph as "not likely to
be a human carcinogen" based on no increased incidence of neoplasms in the rat chronic or
carcinogenicity studies or in the mouse carcinogenicity study.
The toxicology data on dimethomorph provides no indication of enhanced sensitivity of infants
and children based on the results from developmental studies conducted with rats and rabbits as
well as a two-generation reproduction study conducted with rats. In neither the rat
developmental toxicity study nor in the two-generation study were any toxic effects observed at
doses lower than in the parents. No developmental toxicity was demonstrated in the rabbit
developmental toxicity study. EPA determined that the lOx factor to account for enhanced
sensitivity of infants and children be removed based on the available hazard and exposure data
and the following considerations: 1) The developmental and reproductive toxicity data did not
indicate increased susceptibility of rats or rabbits to in utero and/or postnatal exposure to
dimethomorph; 2) The dietary (food only) exposure assessment did not indicate a concern for
potential risk to infants and children as unrefined field study data were used, resulting in an
overestimate of dietary exposure; 3) A worst case modeling scenario to compensate for the
uncertainties in the environmental fate data base resulted in drinking water levels of
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dimethomorph which were less than EPA's level of concern; 4) There are currently no registered
residential uses for dimethomorph.
Chronic dietary (food only) exposure estimates for dimethomorph do not exceed EPA's level of
concern. The most highly exposed population subgroup was
children age 1 to 6 years old at 4 percent of the chronic RfD. In conducting the chronic dietary
risk assessment, EPA made very conservative assumptions: that all commodities having
dimethomorph tolerances will contain residues of dimethomorph, and that these residues will be
at the level of the tolerance. This results in an overestimate of human dietary exposure.
The predicted dimethomorph surface and ground water concentrations are well below EPA's
drinking water level of concern (DWLOC). EPA used the SCI-GROW (Screening Concentration
In Ground Water) model to estimate the Estimated Environmental Concentration (EEC) of
dimethomorph residues in ground water. The reported EEC for dimethomorph residues using
SCI-GROW is 0.26 ppb. EPA used the Generic Estimated Environmental Concentration
(GENEEC) model to estimate acute and chronic EECs of dimethomorph residues in surface
water. The GENEEC model estimated that, with the present use pattern, surface water
concentrations of dimethomorph ranged from a peak of 28 ppb to a 56 day concentration of 24
ppb. EPA's level of concern for chronic exposure to residues of dimethomorph range from 960
ppb for children 1-6 years old to 3400 ppb for the US population and males 13 years and older.
Therefore, exposure from water is below EPA's level of concern for all of the populations
examined. In addition, the aggregate (food and water) chronic exposure for infants, children and
adults does not exceed EPA's level of concern and adverse health effects from chronic exposure
to dimethomorph in food and water are not expected in these populations.
The risk assessment evaluated occupational risk to workers who could be exposed to
dimethomorph through simultaneous dermal and inhalation exposure. Agricultural workers
evaluated in this analysis include ground mixer/loaders, ground applicators, aerial mixer/loaders
and aerial applicators. The dermal and inhalation short-term margin of exposure (MOE) ranged
from 1,200 for aerial mixer/loaders using the wettable powder (WP) to 190,000 for aerial
applicators. The intermediate-term MOEs range from 290 for aerial mixer/loaders using WP to
47,000 for aerial applicators. Exposure from post-application of dimethomorph resulted in
MOEs ranging from 23,000 for short-term to 5,800 for intermediate-term. None of these MOEs
exceed EPA's level of concern (i.e., acceptable MOE > 100) for occupationally exposed workers.
Therefore, these workers are unlikely to experience adverse health effects under the conditions
evaluated.
No residential uses are requested in this petition, nor does dimethomorph have any registered
residential uses; therefore, the risk assessment does not evaluate residential dermal or inhalation
exposures.
EPA has concluded that residue data submitted in support of the tolerance for imported potatoes
indicate that a tolerance level of 0.05 ppm and 0.25 ppm for potatoes, wet peel are adequate
levels for domestic potatoes. A review of domestic field trial data indicates that dimethomorph
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residues do not pose an adverse health risk to humans under the use conditions. Therefore, EPA
has no objection to the establishment of tolerances of 0.05 ppm in or on potatoes and 0.25 ppm
for potatoes, wet peel for residues of the fungicide dimethomorph [(E,Z) 4-[3-(4-chlorophenyl)-
3-(3,4-dimethoxyphenyl)-l-oxo-2-propenyl]morpholine] under 40 CFR 180.493.
Chemical Characteristics of Dimethomorph Technical and Formulations
STUDY NAME ACROBAT TECHNICAL ACROBAT MZ ACROBAT WDG
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Empirical
Formula
Molecular Weight
Color
Physical State
Odor
Melting Point
Density
Solubility
Vapor Pressure
Dissociation
Constant
Octanol/Water
Partition
pH
Stability
Oxidizing or
Reducing Action
Flammability
Explodability
Storage Stability
Viscosity/
C20H22C1N04
375.9
Colorless - Grey
Crystalline solid
Odorless
125 - 149 °C
1.318 g/cm3 at 20°C (pycnometer method)
Solvent Solubility at 20 ° C
water, pH 5 19 mg/L
water, pH 7 18 mg/L
water, pH 9 16 mg/L
n-hexane O.llmg/mL
methanol 39 mg/mL
ethyl acetate 48.3 mg/mL
toluene 49.5 mg/mL
acetone 100 mg/mL
dichloromethane 461 mg/mL
E-isomer: 9.7 x 10 7 Pa at 25°C
Z-isomer: 1.0 x 10 6 Pa at 25 °C
Not determinable (the solubility of
dimethomorph is very low, and the ionized and
unionized forms have identical absorption
coefficients)
E-isomer: K,,w=430 (log Kow=2.63 at 20 °C
Z-isomer: K,,w=543 (log K,,w=2.73 at 20°C
Not applicable - not soluble in water
Thermally and hydrolytically stable
Dimethomorph was determined to have
oxidizing properties in the sense that it can
Not flammable because it could not be ignited
with a flame
When exposed to thermal and mechanical stress,
no reaction was observed, therefore it was
concluded that dimethomorph is not explosive
under conditions of the test.
Stable after 1 year of storage at 25°C in fiber
drums lined with a polypropylene plastic liner.
The percent compositional change was <1%. The
E/Z isomer ratio was stable. Packaging material
remained unchanged. Dimethomorph is
chemically stable when stored at 54°C for 14
days. Decomposition of the test substance was
found to be <1%.
Not applicable - dimethomorph is a solid
C20H22C1N04
Solid
22.69 lbs./cu. ft.
6.89 (2% solution)
Not Applicable
Not Applicable
Not Required
Not Applicable
C20H22C1N04
Solid
40.2 lbs./cu. ft.
6.80 (2% solution)
Some reaction with
potassium
Not Applicable
Not explosive
Data gap - study in
progress
Not Applicable
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Corrosion
Characteristics
I See comments under Storage Stability
|Not corrosive
I Not corrosive
Toxicology Characteristics of Dimethomorph
Acute Toxicity for Acrobat Fungicide Technical
Acute Toxicity Study
Acute Oral - Rats
Acute Oral - Mice
Z-isomer Acute Oral - Rats
E-isomer Acute Oral - Rats
Acute Dermal
Acute Dermal
Acute Inhalation
Primary Eye Irritation
Primary Eye Irritation
Primary Skin irritation
Primary Skin Irritation
Dermal Sensitization
Results
LD5000 mg/kg=F3699 (2402-7927)
mg/kg
LDsn£5000 mg/kg (M,F)
LD5000 mg/kg=F3699 (2402-7927)
mg/kg
LD
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Acute Dermal
Acute Inhalation
Primary Eye Irritation
Primary Eye Irritation
LD,n ^5000 mg/kg
LCsn ^4.24 mg/L
Conjunctival irritation clearing in 4 days
Grade I irritation rlearinp in 48 hrs
IV
III
III
TV
Amte Toxirity for Arrohat M7, Fimpiride
Primary Skin irritation
Primary Skin Irritation
Dermal Sensitization
Grade I irritation at abraded skin sites only,
clearing by Day 2
No irritation reported
Negative in the Magnusson procedure
IV
IV
Not a sensitizer
Acute Toxicity for Acrobat WDG Fungicide
Acute Toxicity Study
Acute Oral - Rats
Acute Oral - Mice
Z-isomer Acute Oral - Rats
E-isomer Acute Oral - Rats
Acute Dermal
Acute Dermal
Acute Inhalation
Primary Eye Irritation
Primary Eye Irritation
Primary Skin irritation
Primary Skin Irritation
Dermal Sensitization
Results
LD5000 mg/kg=F3699 (2402-7927)
mg/kg
LD
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Subchronic Toxicity: In the 90-day rat feeding study, technical grade dimethomorph (98.7 %
a.i.) was administered in the diet to groups of 10 male and 10 female Charles River CD Sprague-
Dawley rats at concentrations of 0, 40, 200, or 1000 ppm (0, 2.9, 14.2, or 73 mg/kg/day for male
rats, and 0, 3.2, 15.8, or 82 mg/kg/day for female rats, respectively) for 13 weeks, 4 days. A
Lowest Observed Adverse Effect Level (LOAEL) was not established because the highest dose
tested produced no biologically significant effects. The No Observed Adverse Effect Level
(NOAEL) is >1000 ppm (73 mg/kg/day for males, and 82 mg/kg/day for females).
In the 90-day dog feeding study, dimethomorph (technical, 96.6% a.i.) was administered to four
male and four female Beagle dogs/dose group in the diet at concentrations of 0, 150, 450, or
1350 ppm (equivalent to doses of 0, 5, 15 or 43 mg/kg/day for males, and 0, 6, 15 or 44
mg/kg/day for females) for 13 weeks. Prostate fibrosis occurred in all four of the high-dose males
but not in any other male. Clinical signs were limited to intermittent incidences of salivation,
lip-licking, tremors, and subdued behavior; these signs were more prevalent in the 150 and 1350
ppm groups but were not considered of toxicologic significance. The critical toxic effect
appeared to be a significant decrease in the mean absolute and relative prostate weights of the
high-dose (1350 ppm) male dogs relative to untreated controls. Therefore, based upon a decrease
in the absolute and relative weights of the prostate and possible threshold liver effects(increased
alkaline phosphatase activity at weeks 6 and 13), the LOAEL is 1350 ppm (43 mg/kg/day). The
NOAEL is 450 ppm (15 mg/kg/day).
Chronic Toxicity: In the rat study, the LOAEL for systemic toxicity was 750 ppm (57.7 mg/kg/
day) for female rats based on decreased body weight and significant increase in the incidence of
"ground glass" foci in the liver and 2000 ppm (99.9 mg/kg/day) for male rats based on decreased
body weight and increased incidence of arteritis. The corresponding NOAEL's are 200 ppm
(11.9 mg/kg/day) for females, and 750 ppm (36.2 mg/kg/day) for males.
In the dog study at 1350 ppm, ALK phosphatase activity was increased throughout the study in
both sexes (245% males, 310% females). The LOAEL for systemic toxicity is 1350 ppm, based
on decreased prostate weight in males. The NOAEL was 450 ppm.
Carcinogenicity: In the rat study, dimethomorph had no significant effect on the development
of neoplasms in male or female rats at the doses tested. Dimethomorph was tested at adequate
doses based on significant decreases in body weight (17% and 13%) and body weight gains (27%
and 14%) in females and males, respectively, in the high dose groups. The LOAEL for systemic
toxicity was 2000 ppm in males and 750 ppm in females. The NOAEL's were 750 ppm (33.9
mg/kg/day) for males and 200 ppm (11.3 mg/kg/day) for females.
In the mouse study, there were no treatment-related increases in the incidence of any neoplastic
lesions. The chemical was adequately tested based on decreased body weight gain (17% and
22% less than control in males and females respectively at 1000 mg/kg/day). The NOAEL for
systemic toxicity was 100 mg/kg/day.
Reproductive Toxicity: In the rat study, the maternal LOAEL =160 mg/kg/day, based on
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decreased mean body weight on gestation days 10-15; decreased body weight gain on gestation
days 10-15, decreased food consumption days 6-15; Maternal NOAEL = 60 mg/kg/day; the
developmental LOAEL =160 mg/kg/day based on increased resorptions; and the developmental
NOAEL = 60 mg/kg/ day.
In the rabbit study, the maternal LOAEL = 650 mg/kg/day based on decreased body weights and
body weight gain; the maternal NOAEL = 300 mg/kg/day. No developmental toxicity was
observed in this study. The developmental NOAEL = 650 mg/kg/day.
In the 2-generation rat reproduction study, the parental toxicity LOAEL = 1000 ppm based on
decreased body weights and body weight gain; the parental NOAEL = 300 ppm (20.8 mg/kg/ day
for males; 24 mg/kg/day for females); the developmental toxicity LOAEL = 1000 ppm based on
delayed incisor eruption at day 10 postpartum; the developmental toxicity NOAEL = 300 ppm;
and the reproductive toxicity NOAEL = 1000 ppm (69 mg/kg/day for males; 79.3 mg/kg/ day for
females).
Mutagenicity: The studies indicate that dimethomorph did not cause gene mutations in
Salmonella or E. Coli bacterial strains, as well as in mammalian gene mutation studies. It was
negative for structural chromosomal aberrations in the mouse micronucleus assay at up to 5000
mg/kg after oral treatment, and up to 200 mg/kg when administered i.p. However,
dimethomorph gave positive responses when tested in CH lung and in human lymphocytes. It
was negative in the cell transformation assay in Syrian hamster embryo cells with and without
activation at up to cytotoxic levels.
Dermal Penetration: Radio-labeled 14C-dimethomorph(97.6%; labeled in the chlorophenyl
ring) was administered dermally to 4 male SD rats/group in water for 8 hours at doses of 7.73
(2.5% w/v aqueous suspension) or 79.62(25% w/v aqueous suspension)mg/kg. Dermal
absorption was 0.05%, 0.07% and 0.27% of the administered dose from rats 4, 8, and 24 hours
after dermal treatment at 7.73 mg/kg, and 0.02%, 0.16% and 0.12% of the dose at 79.62 mg/kg.
Six days after treatment the percent total absorption of the dose in the 7.73 and 79.62 mg/kg was
4.76 and 1.20 percent respectively. Mean percent recovery of the 14C for dose levels of 7.73 and
79.62 mg/kg was 104.1% and 92.1%, respectively.
Neurotoxicity: There are no acute, subchronic, or developmental neurotoxicity studies available
in the data base for dimethomorph. However, in none of the subchronic, chronic, developmental,
or reproduction studies was there any indication that the nervous system was affected by
administration of dimetho-morph. No evidence of neurotoxicity was observed in the available
data base.
General Metabolism: Rat Oral administration of dimethomorph (10 mg/kg single dose; 10
mg/kg 14-day repeated dose; 10 mg/kg 7-day repeated dose; 500 mg/kg single dose) results in
rapid excretion into the urine and feces of rats. For all treatment protocols, most (80-90%) of the
radiolabel administered was excreted in the feces. A considerably smaller amount (6-16%) was
excreted in the urine and only minimal levels (0.1-0.4%) were detected in the organs and tissues.
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Rapid absorption may be inferred by the rapid excretion of metabolites in the urine and bile.
Saturation of absorption following single high doses (500 mg/kg) was indicated by large amounts
(-50%) of radioactivity in the feces being associated with parent compound. For low- or high-
dose treatment, urinary excretion in female rats tended to be greater (up to 2-fold in low-dose
rats) than that of male rats. Retention of dimethomorph or 14C-dimethomorph-derived
radioactivity was generally < 1% for most tissues although the liver exhibited slightly higher
levels (1.4%) and higher levels in the gastrointestinal tract organs were due to radioactivity in the
lumenal contents. Urinary metabolites resulted from demethylation of the dimethoxyphenyl ring
and oxidation of the morpholine ring. Biliary excretion exhibited first-order kinetics with a low-
dose (10 mg/kg) half-life of approximately three hours and a high-dose (500 mg/kg) half-life of
11 hours for males and about 6 hours for females. Biliary metabolites accounted for most of the
fecal excretion following low-dose treatment. The major biliary metabolites were glucuronides
of one and possibly two of the compounds produced by demethylation of the dimethoxyphenyl
ring. The report provided a proposed metabolic pathway for dimethomorph.
Environmental Characteristics
The available environmental fate data for dimethomorph indicates that it is: moderately mobile
in Swiss and standard German soils (Kd 2.09 - 11.67 mL/g and Koc values were 290 - 566);
microbial metabolism is the primary route of dissipation; moderately persistent with aerobic soil
metabolism half-lives of 66 and 117 days in two soils; and no aerobic soil metabolism degradates
were identified other than small amounts of 14CO2; stable to hydrolysis at pH 4, 7 and 9 when
incubated for 10 weeks at 70 and 90 °C. As dimethomorph degraded, most of the radioactivity
was not extracted from the soil. Although it appears that dimethomorph will degrade in
anaerobic aquatic and terrestrial systems, additional data are required to confirm the rates
because the submitted studies had additional carbon sources which may have significantly
accelerated the degradation rates. A pair of isomers of mono-desmethyl dimethomorph were
isolated and identified as primary intermediates for the anaerobic studies. Dimethomorph did not
hydrolyze or photo degrade in the submitted studies.
Ground Water Assessment: The SCI-GROW2 (Screening Concentration In Ground Water)
estimated that ground water concentrations of dimethomorph are not expected to exceed 0.26 ppb
when it is applied at the maximum recommended application rate of 0.20 Ibs. active ingredient
per acre per application with a maximum of five applications. This estimate is determined
primarily by dimethomorph's Freundlich Koc value of 402 used in the model with inputs from
supplemental studies and no monitoring data were used.
Surface Water Assessment: The GENEEC (Generic Estimated Environmental Concentration)
model is a tier one screening model for aquatic pesticide exposure and is used to estimate surface
water concentrations of dimethomorph. Dimethomorph is applied at the maximum
recommended application rate of 0.20 Ibs. a.i./acre with a maximum of five applications. The
application methods for dimethomorph are by chemigation or by ground or aerial application.
The model was run considering an aerial application for a worst case drift scenario with the
following predicted surface water concentrations of dimethomorph: Peak value (acute ) =
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27.7//g/L; average 4-day = 27.48//g/L; average 21-day = 26.25//g/L; average 56-day
(chronic) = 24.40//g/L. Refined surface water modeling (PRZM/EXAMS) was not requested for
the use on potatoes due to the low toxicity to aquatic animals and to the relatively high drinking
water level of concern for dimethomorph used in the drinking water assessment.
Drink Water Assessment: There is no established Maximum Contaminant Level for
dimethomorph in drinking water. No health advisory levels have been established for residues of
dimethomorph in drinking water. The predicted dimethomorph surface and ground water
concentrations are well below EPA's drinking water level of concern (DWLOC). EPA used the
SCI-GROW (Screening Concentration In Ground Water) Model to estimate the Estimated
Environmental Concentration (EEC) of dimethomorph residues in ground water. The reported
EEC for dimethomorph residues using SCI-GROW is 0.26 ppb. EPA used GENEEC (Generic
Estimated Environmental Concentration) model to estimate acute and chronic EECs of
dimethomorph residues in surface water. The GENEEC model estimated that, with the present
use pattern, surface water concentrations of dimethomorph ranged from a peak of 28 ppb to a 56
day concentration of 24 ppb. EPA's level of concern for chronic exposure to residues of
dimethomorph range from 960 ppb for children 1-6 years old to 3400 ppb for the U.S. population
and males 13 years and older. Therefore, exposure from water is below EPA's level of concern
for all of the populations examined.
Ecological Characteristics
The available toxicity data for dimethomorph indicate that it is: practicaly nontoxic to birds on
an acute oral basis (LD50>2,000 mg/kg) and on a subacute dietary basis (LC50>5,300 ppm);
practically nontoxic to mammals based on a rat study (LD50=3,600 mg/kg); practically nontoxic
to honey bees ((LD50>50 //g/bee); moderately toxic on an acute basis to rainbow trout fish (LC50
of 1.5 to 6.2 ppm); slightly toxic to estuarine fish (LC50=11.3 ppm); moderately toxic to
estuarine invertebrates (EC50=5.13 ppm for mollusks and 33 ppm for mysid shrimp.
The available toxicity data for Acrobat® (dimethomorph + mancozeb) shows the mixture is:
very highly toxic to freshwater fish with a (LC50=0.03 ppm dimethomorph concentrations and
0.26 ppm mancozeb); very highly toxic to highly toxic to freshwater invertebrates (LC50=0.08
ppm dimethomorph and 0.73 ppm mancozeb in one supplemental study and LC50=0.41 ppm
dimethomorph and 2.8 ppm mancozeb in a second supplemental study). The concentrations at
which LC50 values for Acrobat® components were determined based on the proportion of
measured dimethomorph and mancozeb. Evaluation of the acute toxicity of Acrobat® to fish
indicates that the LC50 for dimethomorph would be 0.03 ppm if the toxicity of mancozeb,
dimethomorph and the inert ingredients is equal. Based on the LC50 value for rainbow trout,
however, ranging from 1.5 to 6.2 ppm, it appears as though acute toxicity can be attributed
primarily to mancozeb or to synergistic effects from dimethomorph and mancozeb combination.
To estimate risk, data on toxicity of dimethomorph were combined with data on exposure. An
evaluation of the potential risk to nontarget organisms from the use of dimethomorph indicates
low risks to most non-target organisms. Risk quotients for avian organisms were estimated for
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four scenarios distinguished by categories of food items that birds eat: short grass, tall grass,
broadleaf plants and fruits. The chronic LOG trigger for multiple broadcast applications of
dimethomorph is marginally exceeded under the short grass scenario if no degradation is
assumed. Avian chronic risk quotients based on average residues for multiple, broadcast
applications of non-granular products did not exceed the LOG. There is a slight chronic risk to
birds from use of dimethomorph.
SUMMARY OF REGULATORY POSITION AND RATIONALE
Available data provide adequate information to support the conditional registration of
dimethomorph as a technical product (Acrobat Fungicide Technical) and for the two
formulations (Acrobat MZ and Acrobat WDG) for use in or on potatoes at 0.05 ppm and
potatoes, wet peel at 0.25 ppm.
SUMMARY OF DATA GAPS
The following data are required to confirm the information submitted in previous studies: 72-1A
Acute Fish - Bluegill, 72-2A Acute Aquatic Invertebrate, 72-4A/B Freshwater and Estuarine Fish
Early Life Stage, 72-4B Estuarine Aquatic Invertebrate Life Cycle, 162-2 Anaerobic Soil
Metabolism, 162-3 Anaerobic Aquatic Metabolism, Aerobic Aquatic Metabolism, 163-1
Mobility, 164-1 Terrestrial Field Dissipation, 165-1 Confined Rotational Crops, 165-2 Field
Rotational Crops - Wheat (Reserved pending results of confined rotational crop studies), and
165-4 Bioaccumulation in Fish.
Because the potential for synergistic effects between dimethomorph and mancozeb are not clear,
the registrant must (1) submit the following studies on the typical end-use product (TEP):
71-1A/B Acute Avian Oral - Quail/Duck, 71-2A/B Acute Avian Diet - Quail/Duck, 71-4A/B
Avian Reproduction - Quail/Duck, 72-IB Acute Fish Bluegill, 72-3D/E/F Acute
Estuarine/Marine Toxicity - Fish/Mollusk/Shrimp, 72-4B Estuarine Aquatic Invertebrate Life
Cycle, and 72-5 Freshwater Life Cycle Fish, or (2) submit or reference acceptable mancozeb
studies as would be required to support this use pattern and provide a rationale for why TEP
testing would not be necessary, i.e., why the potential for synergistic effects should not be
considered a factor.
CONTACT PERSON AT EPA
Mary L. Waller, Product Manager 21
U.S. Environmental Protection Agency
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Office of Pesticide Programs
Regi strati on Di vi si on (7 5 0 5 C)
Fungicide-Herbicide Branch
401 M St., SW
Washington, DC 20460
Office Location and Phone No.
Room 265, Crystal Mall #2
1921 Jefferson-Davis Hwy.
Arlington, VA 22202
(703) 308-9354
DISCLAIMER: The information presented in this Pesticide Fact Sheet is for informational
purposes only and may not be used to fill data requirements for pesticide registration and
reregi strati on.
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