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EPA REGISTRATION DIVISION COMPANY NOTICE OF FILING FOR 

PESTICIDE PETITIONS PUBLISHED IN THE FEDERAL REGISTER

EPA Registration Division contact: [Shaja Joyner, PM-20, (703)-308-3194]

INSTRUCTIONS: Please utilize this outline in preparing the pesticide petition. In 

cases where the outline element does not apply, please insert “NA-Remove” and 

maintain the outline. Please do not change the margins, font, or format in your 

pesticide petition. Simply replace the instructions that appear in green, i.e., “[insert 

company name],” with the information specific to your action.

TEMPLATE:

[BASF Corporation]

[Insert petition number]

EPA has received a pesticide petition ([insert petition number]) from [BASF 

Corporation], [P.O. Box 13528, Research Triangle Park, North Carolina, 27709]

requesting, pursuant to section 408(d) of the Federal Food, Drug, and Cosmetic Act 

(FFDCA), 21 U.S.C. 346a(d), to amend 40 CFR part 180 by establishing a tolerance for 

residues of [Dimethomorph (BAS 550 F) [(E,Z)4-[3-(4-chlorophenyl)-3-(3,4-

dimethoxyphenyl)-1-oxo-2-propenyl]-morpholine] its metabolites and degradates] in or 

on the raw agricultural commodity [strawberry] at [1.0] parts per million (ppm) and to 

amend 40 CFR part 180 b [replacing] a tolerance for residues of [Dimethomorph (BAS 

550 F) [(E,Z)4-[3-(4-chlorophenyl)-3-(3,4-dimethoxyphenyl)-1-oxo-2-propenyl]-

morpholine] its metabolites and degradates] in or on the raw agricultural commodity

[lettuce, head] from [10] ppm and [lettuce, leaf] at [10] ppm [to 30 ppm]. EPA has 

determined that the petition contains data or information regarding the elements set forth 

in section 408 (d)(2) of FDDCA; however, EPA has not fully evaluated the sufficiency of 

the submitted data at this time or whether the data supports granting of the petition. 

Additional data may be needed before EPA rules on the petition.

A. Residue Chemistry

1. Plant metabolism. [Based upon the results of metabolism studies conducted on 

potato, grape, and lettuce, the nature of the residues in strawberry is considered to be 

understood. The results of the potato metabolism study demonstrated that only negligible 

total radioactive residues (TRR) were found in tubers, 0.01-0.02 parts per million (ppm. 

This is in contrast to the aerial portions of the plant, which were found to have up to 23.5 

ppm TRR, thus demonstrating that translocation of dimethomorph downward within the 

plant was not significant. Almost all of the radioactive residue (97.8%) was extractable 

from the plant at harvest. In the aerial portion of the plant, approximately 70% of the 

TRR was identified as dimethomorph. No metabolites were identified that require 
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regulation.

The results of the grape metabolism study showed that the TRR in/on grapes 

harvested 35 days following the last of four applications [0.8 lb active ingredient per acre 

(ai/A) per application for four consecutive weeks] for a total rate of 3.2 lb ai/A was 14.6 

ppm. Unmetabolized dimethomorph accounted for 87.3% of the TRR (12.7 ppm). No 

metabolites were identified that require regulation.

The results of the lettuce metabolism study showed that the TRR in/on lettuce 

leaves harvested 4 days following the last of 4 applications [approximately 1.0 lb ai/A per 

application with a 9 to 11 day spray interval], for a total rate of 4.1 lb ai/A, was 102 ppm.

Of this total residue, 98.5% was extractable and unmetabolized dimethomorph accounted 

for greater than 93% of the extractable TRR. No metabolites were identified that require 

regulation.

Since the metabolism between the three representative crops is not different, these 

metabolism studies are considered to be adequate to understand the nature of the residue 

in diverse crop groups and as such, an additional metabolism study in strawberries is not 

required.]

2. Analytical method. [A reliable method for the determination of dimethomorph 

residues in plant matrices exists. The determination of the dimethomorph residues in 

strawberries was performed according to the analytical BASF Method No. L0013, 

Method for the determination of geometric isomers of BAS 550 F. The final 

determination of BAS 550 F was performed by LC-MS/MS at a LOQ of 0.005 mg/kg. 

The method has been validated in the context of this residue study.]

3. Magnitude of residues. [Supervised field trials were carried out to determine 

the magnitude of the residue in/on strawberries. The number and locations of field trials 

are in accordance with OCSPP Guideline 860.1500 and Directive 98-02, Section 9. Eight 

field trials were conducted encompassing Regions 1 (PA; 1 trial), 2 (AL; 1 trial), 3 (FL; 1 

trial), 5 (WI; 1 trial), 10 (CA; 3 trials) and 12 (OR; 1 trial) during the 2013 growing 

season. The treated plot at each site received 3 applications of dimethomorph at a rate of 

0.2 lb ai/A for a total seasonal rate of 0.6 lb ai/A with a PHI of 0 days after the last 

application. Detected residues of Dimethomorph in strawberries support the proposed

tolerance.]

B. Toxicological Profile

1. Acute toxicity.

[i. Oral LD50 studies were conducted on dimethomorph technical: 

a. An acute oral toxicity study in the Sprague-Dawley rat for dimethomorph 

technical with a LD50 of 4,300 milligrams/kilogram body weight (mg/kg 

b.w.) for males and 3,500 mg/kg b.w. for females. Based upon EPA toxicity

criteria, the acute oral toxicity category for dimethomorph technical is 

Category III or slightly toxic.

b. An acute toxicity study in the CD-1 mouse for dimethomorph technical with 

a LD50 of greater than 5000 mg/kg b.w. for males and 3699 mg/kg/b.w. for 

females. Based on the EPA toxicity category criteria, the acute oral toxicity
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category for dimethomorph technical is Category III or slightly toxic.

ii. Oral LD50 studies were conducted on the two isomers (E and Z) alone:

c. An acute oral toxicity study in the Wistar rat for the E-isomer with a LD50

greater than 5,000 mg/kg b.w. for males and approximately 5,000 mg/kg b.w. 

for females. 

d. An acute oral toxicity study in the Wistar rat for the Z-isomer with a LD50

greater than 5,000 mg/kg b.w. for both males and females.

iii. An acute dermal toxicity study in the Wistar rat for dimethomorph technical with 

a dermal LD50 greater than 5,000 mg/kg b.w. for both males and females. Based on 

the EPA toxicity category criteria, the acute dermal toxicity category for 

dimethomorph is Category IV or relatively non-toxic.

iv. A 4-hour inhalation study in Wistar rats for dimethomorph technical with a LC50 

greater than 4.2 mg/L for both males and females. Based on the EPA toxicity 

category criteria, the acute inhalation toxicity category for dimethomorph technical 

is Category IV or relatively non-toxic.

v. A skin irritation study was performed using New Zealand White rabbits. Based on 

the EPA toxicity criteria, the skin irritation toxicity category for dimethomorph 

technical in this study is Category IV or non-to-slightly irritating.

vi. An eye irritation study using New Zealand White rabbits demonstrated 

dimethomorph technical produced moderate conjunctival redness, slight to 

moderate chemosis and slight discharge three hours after treatment. Based on the 

EPA toxicity criteria, the eye irritation category for dimethomorph technical is 

Category III (slightly-to-moderately irritating).]

2. Genotoxicty.

[i. Salmonella reverse gene mutation assays (2 studies) were negative up to a limit 

dose of 5,000 g/plate. Chinese hamster lung V79 cells were negative for 

mutations at the HGPRT locus at up to cytotoxic doses in two studies.

ii. Structural Chromosomal Aberration studies were presumptively weakly positive in 

human lymphocytic cultures, but only in S9 activated cultures treated at 422 

g/ml, the highest dose tested (HDT), which was strongly cytotoxic. No increase 

in chromosomal aberrations was observed in the absence of S9 activation at all 

doses. Furthermore, the positive clastogenic response observed under the in vitro 

conditions was not confirmed in two in vivo micronucleus assays.

iii. Micronucleus assay (2 studies) indicated that dimethomorph was negative for 

inducing micronuclei in bone marrow cells of mice following i.p. administration of 

doses up to 200 mg/kg or oral doses up to the limit dose of 5,000 mg/kg. Thus, 

dimethomorph was found to be negative in these studies for causing cytogenetic 

damage in vivo.

iv. Dimethomorph was negative for transformation in Syrian hamster embryo cells 

treated, in the presence and absence of activation, up to cytotoxic concentrations 

(265 g/ml/+S9; 50 g/ml/-S9).]

3. Reproductive and developmental toxicity.

[i. A rat developmental toxicity study with a Lowest-Observed-Effect Level (LOEL) 

for maternal toxicity of 160 mg/kg/day and a No-Observed-Effect Level (NOEL) 

for maternal toxicity of 60 mg/kg/day. The NOEL for developmental toxicity is 60 
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mg/kg/day. Dimethomorph is not teratogenic in the Sprague-Dawley rat.

ii. A rabbit development toxicity study with a LOEL for maternal toxicity of 650 

mg/kg/day and a NOEL for maternal toxicity of 300 mg/kg/day. The NOEL for 

developmental toxicity is 650 mg/kg/day, the highest dose tested. Dimethomorph 

is not teratogenic in the New Zealand white rabbit.

iii. A two-generation rat reproduction study with a LOEL for parental systemic 

toxicity of 1000 ppm, or approximately 80 mg/kg/day, and a NOEL for parental 

systemic toxicity of 300 ppm, or approximately 24 mg/kg/day. The NOEL for 

fertility and reproductive function was 1000 ppm, the highest concentration tested, 

or approximately 80 mg/kg b.w./day.]

4. Subchronic toxicity.

[i. A 90-day dietary study in Sprague-Dawley rats with a NOEL of greater than or 

equal to 1000 ppm, the highest concentration tested, or approximately 73 

mg/kg/day for males and 82 mg/kg/day for females.

ii. A 90-day dog dietary study with a NOEL of 450 ppm, or approximately 15 

mg/kg/day, and a LOEL of 1350 ppm, or approximately 43 mg/kg/day.]

5. Chronic toxicity.

[i. A 2-year chronic toxicity study in Sprague-Dawley rats with a NOEL of 150 ppm 

or approximately 9.4 mg/kg/day for males and 11.9 mg/kg/day for females. The 

LOEL for systemic toxicity is 450 ppm, or approximately 36.2 mg/kg/day for 

males and 57.7 mg/kg/day for females.

ii. A 1-year chronic toxicity study in dogs with a NOEL of 450 ppm, or 

approximately 14.7 mg/kg/day and a LOEL of 1350 ppm, or approximately 44.6 

mg/kg/day.

iii. A 2-year oncogenicity study in Sprague-Dawley rats with a NOEL for systemic 

toxicity of 200 ppm, or approximately 8.8 mg/kg/day for males and 11.3 

mg/kg/day for females. The LOEL for systemic toxicity was 750 ppm, or 

approximately 33.9 mg/kg/day for males and 46.3 mg/kg/day for females. There 

was no evidence of increased incidence of neoplastic lesions in treated animals. 

The NOEL for oncogenicity is 2000 ppm, the highest concentration tested, or 

approximately 94.6 mg/kg/day for males and 132.5 mg/kg/day for females.

iv. A 2-year oncogenicity study in CD-1 mice with a NOEL for systemic toxicity of 

100 mg/kg/day and a LOEL of 1,000 mg/kg/day. There was no evidence of 

increased incidence of neoplastic lesions in treated animals. The NOEL for 

oncogenicity is 1,000 mg/kg/day, the highest dose tested.

v. A subchronic neurotoxicity study in Wistar rats with a NOEL of 432.9 mg/kg/day

in males or 510.1 mg/kg/day in females. There was no evidence of neurotoxicity.

vi. A subchronic immunotoxicity study in male Wistar rats with a NOEL of 2400 

ppm, equivalent to 184 mg/kg/day 432.9 mg/kg/day. There was no evidence of an 

immunotoxic potential.]

6. Animal metabolism. [Results from the livestock and rat metabolism studies 

show that orally administered dimethomorph was rapidly excreted by the animals. The 

principal route of elimination is via the feces.]
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7. Metabolite toxicology. [There were no metabolites identified in plant or animal 

commodities which require regulation.]

8. Endocrine disruption. [Collective organ weights and histopathological findings 

from the two-generation reproduction study in rats, as well as from the subchronic and 

chronic toxicity studies in two or more animal species, demonstrate no apparent 

estrogenic effects or effects on the endocrine system. There is no information available 

that suggests that dimethomorph technical would be associated with endocrine effects.]

C. Aggregate Exposure

1. Dietary exposure. [An assessment was conducted to evaluate the potential risk 

due to chronic dietary exposure of the U.S. population and sub-populations to residues of 

dimethomorph. This analysis included all currently proposed tolerances listed in U.S. 40 

CFR § 180.493 and the proposed tolerance for strawberry at 1.0 ppm.]

i. Food. [Acute Dietary Exposure Assessment

An acute assessment was not needed since the U.S. EPA Toxicological Endpoint 

Selection (TES) Committees had previously evaluated the dimethomorph toxicity data, 

and determined there was no toxicological endpoint attributable to a single dose and a 

quantitative acute dietary exposure and risk assessment are not required. 

Chronic Dietary Exposure Assessment

A Tier 1 chronic dietary exposure assessment was conducted assuming tolerance level 

residues and 100% crop treated factors for all registered crops and the proposed new use

for strawberry. The EPA Food Commodity Ingredient Database (FCID) was also used in 

Exponent's Dietary Exposure Evaluation Module (DEEM-FCID) software. Tolerances for 

animal commodities (i.e. meat, meat byproducts, milk, eggs) are not required since 

metabolism studies have shown dimethomorph residues will not occur in animal 

commodities from the consumption of dimethomorph residues in livestock feed. 

Furthermore, there are no livestock feedstuffs associated with strawberry. Therefore, 

dimethomorph tolerances for residues in animal commodities do not need to be 

established.

Dietary exposure estimates (food + drinking water) were compared against the 

established dimethomorph chronic Population Adjusted Dose (cPAD) of 0.11 mg/kg 

b.w./day for all populations. Results of the chronic dietary assessments are listed in the 

table below. The estimated chronic dietary exposure from crops (both established and 

proposed tolerances) was less than 25% of the cPAD for all subpopulations (Table 1). 

Additional refinements such as the use of anticipated residues and crop treatment factors 

would further reduce the estimated chronic dietary exposure. The results in the Table 

below demonstrate that there are no risk concerns for any subpopulation based on 

established and new strawberry, and that the results clearly meet the FQPA standard of 

reasonable certainty of no harm.

Table 1. Summary of Chronic Dietary Exposure Assessment considering crops with 

established and proposed tolerances for Dimethomorph and drinking water.
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Population sub-group

Chronic Exposure 

(mg/kg bw/day) %cPAD

US Population 0.012933 11.8

All infants (< 1 year) 0.010746 9.8

Children 1-2 0.026544 24.1

Children 3-5 0.022276 20.3

Children 6-12 0.012695 11.5

Youth 13-19 0.008745 8.0

Adults 20-49 0.012406 11.3

Adults 50+ yrs 0.012718 11.6

Females 13 - 49 yrs 0.01202 10.9

]

ii. Drinking water. [The chronic drinking water values used in this analysis were 

the values proposed by EPA, September 15, 2011, “Dimethomorph: Human Health Risk 

Assessment to Support Amended Use on Grapes, Bulb Vegetables, Leafy Brassica 

Vegetables and Leafy Vegetables”. The chronic drinking water value used was 24.7 ug/L. 

Acute Aggregate Exposure and Risk (Food and water)

The U.S. EPA Toxicological Endpoint Selection (TES) Committees has evaluated the 

dimethomorph toxicity data and determined there was no endpoint attributable to a single 

dose, therefore an acute aggregate exposure and risk evaluation is not required. 

Chronic Aggregate Exposure and Risk (food and water)

The aggregate chronic risk includes residues of dimethomorph from food and water. The 

results in Table 1 demonstrate there are no risk concerns for any subpopulation based on 

established and new uses, and that the results clearly meet the FQPA standard of 

reasonable certainty of no harm.]

2. Non-dietary exposure. [Dimethomorph is not registered for use on any sites that 

would result in residential exposure. Therefore, a residential exposure and risk 

assessment was not conducted. Also, a short-term aggregate risk assessment is not 

required. ]

D. Cumulative Effects

[There is no information to indicate that any toxic effects produced by

dimethomorph would be cumulative with those of any other chemical. The fungicidal 

mode of action of dimethomorph is unique; dimethomorph inhibits cell wall formation 

only in Oomycete fungi. The result is lysis of the cell wall that kills growing cells and

inhibits spore formation in mature hyphae. This unique mode of action and limited pest 

spectrum suggest that there is little or no potential for cumulative toxic effects in 

mammals. In addition, the toxicity studies submitted to support this petition do not 

indicate that dimethomorph is a particularly toxic compound. No toxic end-points of 
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potential concern were identified.]

E. Safety Determination

1. U.S. population. [Based on this risk assessment, BASF concludes that there is a 

reasonable certainty that no risk concerns to the general population from the aggregate 

exposure to dimethomorph residues.]

2. Infants and children. [Based on this risk assessment, BASF concludes that 

there is a reasonable certainty that no risk concerns to infants or children from the 

aggregate exposure to dimethomorph residues.]

F. International Tolerances

[There are no Canadian, Mexican, or Codex MRLs established for dimethomorph 

for strawberry; consequently, a discussion of international harmonization is not relevant.]