UNITED STATES ENVIRONMENTAL PROTECTION 

AGENCY 

WASHINGTON D.C., 20460 

Chemical Code: 036602 

DP Barcode: 328531, 337542, 338102 

MEMORANDUM July 30, 2007 

SUBJECT: EFED risk assessment for the registration of the new chemical 

Mandipropamid 

TO: Tony Kish, Risk Manager 

Registration Division (7505P) 

FROM: Fred Jenkins, MS, Biologist

Ibrahim Abdel-Saheb, Ph.D., Environmental Scientist 

Ron Dean, MS, Biologist 

Environmental Risk Branch II 

Environmental Fate and Effects Division 

THROUGH: Dana Spatz, Branch Chief (acting) 

Environmental Risk Branch II 

Environmental Fate and Effects Division (7507P) 

EFED has completed the screening level ecological risk assessment for the registration of 

the new chemical, mandipropamid. The risk assessment has been conducted in 

accordance with the Agency’s Guidelines for Ecological Risk Assessment, and is in 

compliance with the paper titled “Overview of the Ecological Risk Assessment Process in 

the Office of Pesticide Programs, U.S. Environmental Protection Agency” (“Overview 

Document”) (January 2004). 
Risks Conclusions 

Based on the available data, EFED has determined that mandipropamid’s proposed uses 

are not expected to pose significant: 

• acute or chronic risk to birds 

• acute or chronic risk to mammals 

• acute risk to aquatic invertebrates 

• chronic risk to fish 

• acute risk to terrestrial or aquatic plants 

EFED is unable to access the acute risk of mandipropamid to fish and mammals, and the 

chronic risks to aquatic invertebrates because all the fish acute toxicity data are deemed 

invalid, the mammal acute toxicity data were not submitted, and the chronic aquatic 

invertebrate toxicity data are deemed invalid. 

Recommended Label Statements 

Based on the use pattern of mandipropamide EFED recommends that the following 

statement be applied to the mandipropamide end-use product label. 

Recommended Label Statements: 

“This product may contaminate water through drift of spray in wind. This product has “a 

potential for runoff” for “several months or more after application.” Poorly draining soils 

and soils with shallow water tables are more prone to produce runoff that contains this 

product. A level, well maintained vegetative buffer strip between areas to which this 

product is applied and surface water features such as ponds, streams, and springs will 

reduce the potential for contamination of water from rainfall-runoff. Runoff of this 

product will be reduced by avoiding applications when rainfall is forecasted to occur 

within 48 hours.” 

“Do not apply directly to water, or to areas where surface water is present or to intertidal 

areas below the mean high water mark. Do not contaminate water when disposing of 

equipment washwater or rinsate." 

ii
Uncertainties and Data Gaps

The following provides a summary of the data gaps in this assessment. 

Assessment Data Gaps: 

• Fish acute toxicity: All data submitted are invalid. The studies were invalidated because 

the dissolved mandipropamid concentration was not determined (test solutions contained 

undissolved particulate test material and the measured concentrations were significantly 

unstable throughout the testing). Therefore, it is not possible to obtain accurate toxicity 

endpoint values that could be used for risk assessment purposes. 

• Invertebrate chronic toxicity: The submitted study is invalid because reproduction of the 

daphnids in the solvent control was significantly lower than in the negative control. 

Risk Mitigation Options

Since this screening level risk assessment has demonstrated that the proposed use of 

mandipropamid is not expected to pose any significant risks above the Agency’s Level of 

Concern (LOC), EFED does not currently believe that any additional risk mitigation 

measures are needed. 

iii
Table of Contents 

I. EXECUTIVE SUMMARY .................................................................................................... 7 

A. Nature of Chemical Stressor............................................................................................... 7 

B. Potential Risks to Non-Target Organisms.......................................................................... 7 

C. Conclusions – Exposure Characterization .......................................................................... 8 

D. Conclusions – Effects Characterization.............................................................................. 8 

E. Uncertainties and Data Gaps............................................................................................... 9 

II. PROBLEM FORMULATION ............................................................................................. 11 

A. Stressor Source and Distribution ...................................................................................... 11 

1. Source and Intensity.................................................................................................... 11 

2. Physical/Chemical/Fate and Transport Properties........................................................ 11 

3. Pesticide Type, Class, and Mode of Action.................................................................. 14 

4. Overview of Pesticide Usage........................................................................................ 14 

B. Receptors .......................................................................................................................... 14 

1. Aquatic Effects............. ............................................................................................ 15 

2. Terrestrial Effects.......... ............................................................................................ 16 

3. Ecosystems at Risk......... ........................................................................................... 16 

C. Assessment Endpoints ...................................................................................................... 19 

D. Conceptual Model............................................................................................................. 19 

1. Risk Hypotheses............ ........................................................................................... 20 

2. Diagram...................... ........................................................................................... 20 

E. Analysis Plan .................................................................................................................... 21 

1. Preliminary Identification of Data Gaps and Methods................................................. 21 

2. Measures to Evaluate Risk Hypotheses and Conceptual Model................................... 21 

a. Measures of Exposure............................................................................................... 21 

b. Measures of Effect.................................................................................................... 22 

c. Measures of Ecosystem and Receptor Characteristics ............................................. 22 

III. ANALYSIS........................................................................................................................... 24 

A. Use Characterization......................................................................................................... 24 

B. Exposure Characterization................................................................................................ 25 

1. Environmental Fate and Transport Characterization.................................................... 25 

a. Summary of Empirical Data ..................................................................................... 25 

b. Degradation and Metabolism.................................................................................... 26 

c. Transport and Mobility ............................................................................................. 26 

d. Field Studies ............................................................................................................. 27 

2. Measures of Exposure................................................................................................. 27 

a. Aquatic Exposure Modeling ..................................................................................... 27 

b. Aquatic Exposure Monitoring and Field Data.......................................................... 28 

3. Measures of Terrestrial Exposures ............................................................................... 28 

a. Terrestrial Exposure Modeling ................................................................................. 28 

b. Terrestrial Residue Studies....................................................................................... 32 

C. Ecological Effects Characterization.................................................................................. 32 

1. Aquatic Effects Characterization.................................................................................. 32 

iv
a. Aquatic Animals ....................................................................................................... 36 

(1). Acute Effects..................................................................................................... 36 

(2). Chronic Effects................................................................................................. 37 

(3). Sublethal Effects............................................................................................... 39 

(4). Field Studies ..................................................................................................... 39 

b. Plants Inhabiting Aquatic Areas............................................................................... 39 

2. Terrestrial Effects Characterization.............................................................................. 40 

a. Terrestrial Animals................................................................................................... 43 

(1). Acute Effects..................................................................................................... 43 

(2). Chronic Effects................................................................................................. 44 

(3). Sublethal Effects............................................................................................... 45 

(4). Field Studies ..................................................................................................... 46 

b. Terrestrial Plants....................................................................................................... 46 

IV. RISK CHARACTERIZATION............................................................................................ 48 

A. Risk Estimation – Integration of Exposure and Effects Data ........................................... 48 

1. Non-Target Aquatic Animals and Plants..................................................................... 48 

a. Acute Risk to Aquatic Animals................................................................................ 48 

b. Chronic Risk to Aquatic Animals............................................................................. 49 

c. Risks to Aquatic Plants............................................................................................. 50 

2. Non-Target Terrestrial Animals................................................................................... 50 

a. Acute Risk to Mammals and Birds........................................................................... 50 

b. Chronic Risk to Birds and Mammals........................................................................ 50 

c. Risk to Terrestrial Invertebrates ............................................................................... 51 

3. Non-target Plants Inhabiting Terrestrial and Semi-Aquatic Areas............................... 51 

B. Risk Description ............................................................................................................... 52 

1. Risks to Aquatic Organisms ......................................................................................... 52 

2. Risks to Terrestrial Organisms ................................................................................. 52 

a. Terrestrial Animals (Mammals and Birds)............................................................... 52 

b. Insects ....................................................................................................................... 53 

c. Plants......................................................................................................................... 53 

3. Review of Incident Data... ........................................................................................... 53 

4. Endocrine Effects....................................................................................................... 53 

C. Federally Threatened and Endangered (Listed) Species Concerns .............................. 54 

1. Action Area............................................................................................................. 54 

2. Taxonomic Groups Potentially at Risk......................................................................... 54 

3. Probit Dose Response Relationship............................................................................. 55 

4. Indirect Effects Analysis.............................................................................................. 55 

5. Critical Habitat.......................................................................................................... 55 

D. Description of Assumptions, Limitations, Uncertainties, Strengths and Data Gaps........ 56 

1. Assumptions, Limitations, Uncertainties, Strengths and Data Gaps Related to Exposure 

for All Taxa.................................................................................................................... 56 

2. Assumptions, Limitations, Uncertainties, Strengths and Data Gaps Related to Exposure 

for Aquatic Species.......................................................................................................... 56 

v
vi

a. GENEEC Standard Runoff Model............................................................................ 56 

3. Assumptions, Limitations, Uncertainties, Strengths and Data Gaps Related to Exposure 

for Terrestrial Species....................................................................................................... 57 

a. Residue Concentration.............................................................................................. 57 

b. Variation in Habitat and Dietary Requirements ....................................................... 57 

c. Variation in Diet Composition.................................................................................. 57 

d. Exposure Routes Other than Dietary ........................................................................ 58 

e. Incidental Soil Ingestion Exposure ........................................................................... 58 

f. Inhalation Exposure .................................................................................................. 58 

g. Dermal Exposure ...................................................................................................... 58 

h. Drinking Water Exposure ......................................................................................... 67

i. Dietary Intake – Differences Between Laboratory and Field Conditions ................ 59 

4. Assumptions, Limitations, Uncertainties, Strengths and Data Gaps Related to Effects 

Assessment.................................................................................................................... 60 

a. Age Class and Sensitivity of Effects Thresholds...................................................... 60 

b. Use of the Most Sensitive Species Tested ................................................................ 61 

V. REFERENCES ..................................................................................................................... 62 
7

I. EXECUTIVE SUMMARY 

A. Nature of Chemical Stressor 

Mandipropamid is a new fungicide intended for the control of foliar oomycete pathogens in a 

range of crops. Mandipropamid’s mode of action is as a preventive foliar fungicide that is 

effective at inhibiting spore germination, mycelial growth and sporulation. Mandipropamid 

is absorbed to the plant wax layer, providing resistance to rainwater wash-off. Once 

mandipropamid is taken up by the plant tissue, translaminar mobility provides protection of 

the opposition leaf surface. 

In accordance with the registrant submitted label, the proposed maximum use rate for all 

crops is four applications of 0.13 lbs a.i./acre with 7-10 days between each application. 

Mandipropamid is formulated as a suspension concentrate that requires the use of an external 

adjuvant (such as a non-ionic surfactant, crop oil concentrate, silicone based, or blend 

methylated or ethylated seed oil) to enhance fungicidal activity. 

C. Potential Risks to Non-Target Organisms 

Based on the available data, EFED has determined that mandipropamid’s proposed uses are 

not expected to pose significant: 

• acute or chronic risk to birds 

• acute or chronic risk to mammals 

• acute risk to aquatic invertebrates 

• chronic risk to fish 

• acute risk to terrestrial or aquatic plants 

EFED is unable to access the acute risk of mandipropamid to fish and the chronic risks to 

aquatic invertebrates because all the fish acute toxicity data are deemed invalid and the 

chronic aquatic invertebrate toxicity data are deemed invalid as well. 
8

Table 1 summarizes the conclusions of this assessment in regards to endangered species. 

Table 1. Summary of Screening Level Risk Assessment Findings in Regards to Direct and 

Indirect Effects of Mandipropamid to Federally Listed Species. 

Listed Taxon Direct Effects Indirect Effects

Terrestrial and semi-aquatic plants - monocots No No 

Terrestrial and semi-aquatic plants - dicots No No

Terrestrial invertebrates No No

Birds No No

Terrestrial-phase amphibians No No

Reptiles No No

Mammals No 

Aquatic non-vascular plants No No 

Aquatic vascular plants No No 

Freshwater fish No data No 

Aquatic-phase amphibians No No 

Freshwater crustaceans No No 

Mollusks No No 

Marine/estuarine fish No No 

Marine/estuarine crustaceans No No 

C. Conclusions – Exposure Characterization 

Aquatic and terrestrial species may be exposed to mandipropamid through its proposed 

agricultural uses. Mandipropamid is considered to be persistent in the environment. 

Mandipropamid appears to be stable to hydrolysis at environmental pH (pH range 5–9) but 

susceptible to photolysis in soil and water. Based on its vapor pressure and Henry’s Law 

constant, volatilization from water and soil are not expected to be important environmental 

fate processes. Mandipropamid is moderately mobile in soil and has the potential to leach 

into ground water. The stressors of concern are the parent chemical, mandipropamid, and its’ 

degradates SYN500003 and SYN504851 both of which were identified by the Human Health 

Effects Division (HED) as toxic degradates of concern. 

D. Conclusions – Effects Characterization 

Fish Acute Toxicity 

No acceptable fish acute toxicity data are available. The studies submitted are invalid (See 

Appendix E for further details). 

Fish Chronic Toxicity 

The registrant submitted a freshwater fish chronic toxicity study that demonstrates chronic 

exposure to technical mandipropamid causes significant decreases to fish growth at a 
9

NOAEC and LOAEC concentration of 0.21 ppm and 0.45 ppm respectively (See Appendix E 

for further details). 

Aquatic Invertebrate Toxicity

The registrant submitted aquatic invertebrate acute toxicity studies demonstrate that technical 

mandipropamid is moderately toxic to freshwater invertebrates and very highly to moderately 

toxic marine/estuarine invertebrates (See Appendix E for further details). 

Aquatic Invertebrate Chronic Toxicity 

The registrant submitted aquatic invertebrate chronic toxicity data are invalid (See Appendix 

E for further details). 

Plant Toxicity 

i. Terrestrial Plants

The registrant submitted a vegetative vigor terrestrial plant toxicity study and a seedling 

emergence terrestrial plant toxicity study. Both studies demonstrate that the measured 

endpoints did not reach the EC25 toxicity level in any of species tested with the exception of 

the carrot species, which rendered unreliable results in the seedling emergence study (See 

Appendix E for further details). The monocot and dicot NOAEC values for the seedling 

emergence studies are 0.660 lbs a.i./A and 0.165 lbs a.i./A respectively. The monocot and 

dicot NOAEC values for the vegetative vigor studies are 0.198 lbs a.i./A and 0.792 lbs a.i./A 

respectively. 

ii. Aquatic Plant Toxicity

The registrant has submitted a nonvascular aquatic plant toxicity study testing the effect of 

mandipropamid on the green alga, Pseudokirchneriella subcapitata (MRID 468001-21) and a 

vascular aquatic plant toxicity study testing the effect of mandipropamid on Lemna gibba

(MRID 468001-19). The green algal study demonstrates an EC50 > 2.5 ppm a.i. for all 

endpoints measured and a NOAEC of 1.3 ppm based on biomass. The Lemna gibba study 

demonstrates an EC50 > 7.9 ppm a.i. for all endpoints measured and a NOAEC of 1.3 based 

on growth rate. (See Appendix E for further details). 

E. Uncertainties and Data Gaps

The following provides a summary of the data gaps in this assessment. 

Assessment Data Gaps: 

• Fish acute toxicity: All data submitted are invalid. The studies were 

invalidated because the dissolved mandipropamid concentration was not 
10

determined (test solutions contained undissolved particulate test material and 

the measured concentrations were significantly unstable throughout the 

testing). Therefore, it is not possible to obtain accurate toxicity endpoint 

values that could be used for risk assessment purposes. 

• Invertebrate chronic toxicity: The submitted study is invalid because 

reproduction of the solvent control daphnids was significantly lower than that 

of negative control daphnids.
11

II. PROBLEM FORMULATION 

A. Stressor Source and Distribution 

1. Source and Intensity 

Mandipropamid, a fungicide (proposed name RevusTM), is specifically intended to control 

foliar oomycete pathogens in a range of crops. Mandipropamid is not currently registered for 

agricultural use in the U.S. This chemical is applied to crops via ground and aerial methods. 

This assessment focuses on the proposed uses of mandipropamid on brassica vegetables, bulb 

vegetables, cucurbits, fruiting vegetables, grapes, leafy vegetables, potatoes, tomatoes, 

tuberous and corm vegetables. 

2. Physical/Chemical/Fate and Transport Properties 

 Mandipropamid is considered to be persistent in the environment. The major route of 

dissipation is degradation under aerobic aquatic conditions. Mandipropamid degrades to 

several intermediatery degradation products. The transformation products are ultimately 

degraded to non-extractable residues and carbon dioxide. Mandipropamid is moderately 

mobile and some of its metabolites are mobile to highly mobile in soils, and therefore have 

the potential to leach into ground water. Mandipropamid can reach surface waters via spray 

drift and rainfall events that cause runoff. The important physical and chemical properties 

for mandipropamid are summarized in Table 2 followed by its chemical structure (Figure 1).
12

Table 2. Chemical and Physical Properties for Mandipropamid 

CAS number 374726-62-2 MRID 46800009 

SMILES notation Clc1ccc(cc1)C(OCC#C)C(=O)NCC

c1ccc(c(c1)OC)OCC#C 

(ISIS v2.3/Universal SMILES). 

C1=C(Cl)C=CC(C(OCC#C)C(=O)

NCCC2=CC=C(OCC#C)C(OC)=C

2)=C1 (EPI Suite, v3.12 SMILES). 

C1c(ccc(c1)C(C(NCCc1ccc(c(c1)O

C)OCC#C)=O)OCC#C)C1 

MRID 46800009 

Molecular weight 411.9 MRID 46800009 

Molecular formula C23H22ClNO4 MRID 46800009 

Vapor pressure 3.52 X 10-8 Torr MRID 46800007&8 

Solubility in water (pH 7, 20 oC) 2.3 ppm MRID 46800009 

Henry’s Law constant 

8.293E-09 (atm.m3/mole) 

Calculated from Vp, Solubility, and 

M.wt 

Log Kow 3.13 MRID 46800007&8 

pKa Not reported 

Hydrolysis half-life (days) for pH 5, 

7, and 9 

Stable at pH 5, 7, and 9 MRID 46800007&8 

Aquatic photolysis half-life 0.63 -1.1 days MRID# 46800009,10,13,14 

Soil photolysis half-life 16.4 – 24 days MRID 46800015,16,17 

Aerobic soil metabolism half-life 72.2 days (sandy loam) 

26.1days (silt loam) 

78 - 103 days (silt loam) 

32.4 days (loan, silt loam) 

51.3 days (sandy clay loam, ) 

90 days (loam) 

83.5 (loamy sand) 

MRID 46800020,21 

MRID 46800022 

MRID 46800024,25 

MRID 46800027 

MRID 46800028 

Anaerobic soil metabolism half-life 151 MRID 46800022 

Koc (adsorption) 782 (Loam/silt loam ) 

1294 (Loamy sand ) 

1067 (Silty clay loam ) 

1064 (Silt loam ) 

694 (sandy loam) 

405 (loamy sand) 

624 (loamy sand) 

MRID 46800038,39 

MRID 46800040,41 

Aerobic aquatic metabolism halflife 17.7 days MRID 46800030,31 

Anaerobic aquatic metabolism halflife No data available Unacceptable study (MRID 

466800033,34) 
13

Cl

O

O

N

2CH

C

CH

C

H2

C

H2

O

O CH3

C

H2

C

CH

Mandipropamid 

Cl

O

O

OH

CH2

C

CH3

SYN500003 

Cl

O

O

OH

2CH

C

SYN504851 

Figure 1. Chemical Structures of Mandipropamid and its major degradates. 
14

3. Pesticide Type, Class, and Mode of Action 

Mandipropamid belongs to the new mandelamide chemical class of fungicides. 

Mandipropamid’s mode of action is as a preventive foliar fungicide that is effective at 

inhibiting spore germination, mycelial growth and sporulation. Mandipropamid is absorbed 

to the plant wax layer, providing resistance to rainwater wash-off. Once mandipropamid is 

taken up by the plant tissue, translaminar mobility provides protection of the opposition leaf 

surface. 

4. Overview of Pesticide Usage 

The proposed label specifies that mandipropamid is a ground and aerially applied fungicide 

formulated as a suspension concentrate that requires the use of an external adjuvant. 

The proposed label specifies that the maximum amount of mandipropamid that may be used 

per growing season is 0.52 lbs a.i./acre which may be divided into 4 applications of 0.13 lbs 

a.i./acre with a 7-day minimum interval between each application. 

Actual pesticide usage data are not available since this chemical is currently not registered 

for use in the US. Because this chemical is proposed for use on field brassica vegetables, 

bulb vegetables, cucurbits, fruiting vegetables, grapes, leafy vegetables, potatoes, tomatoes, 

tuberous and corm vegetables, the current geographic distribution of these crops is expected 

to be generally representative of potential mandipropamid application areas. 

B. Receptors 

Each assessment endpoint requires one or more measures of ecological effect, which are 

defined as changes in the attributes of an assessment endpoint itself or changes in a surrogate 

entity or attribute in response to exposure to a pesticide. Ecological measures of effect for 

the screening level risk assessment are based on a suite of registrant-submitted toxicity 

studies performed on a limited number of organisms in broad groupings listed in Table 3. 

Table 3. Taxonomic Groups and Test Species Evaluated for Ecological Effects in 

Screening-Level Risk Assessments 

Taxonomic Group Example(s) of Representative Species 

Birds a Mallard duck (Anas platyrhynchos) 

Bobwhite quail (Colinus virginianus) 

Mammals Laboratory rat (Rattus norvegicus) 

Freshwater fish b Bluegill sunfish (Lepomis macrochirus) 

Rainbow trout (Oncorhynchus mykiss) 

Freshwater invertebrates Water flea (Daphnia magna) 

Estuarine/marine fish Sheepshead minnow (Cyprinodon variegatus) 

Estuarine/marine invertebrates Eastern oyster (Crassostrea virginica) 

Mysid shrimp (Americamysis bahia) 

Terrestrial plants Monocot and dicot 

Insects Honeybee 
15

Table 3. Taxonomic Groups and Test Species Evaluated for Ecological Effects in 

Screening-Level Risk Assessments 

Taxonomic Group Example(s) of Representative Species 

Aquatic plants Bluegreen alga 

Green alga 

Saltwater diatom 

Duckweed (Lemna gibba) a

 Birds are considered surrogates for amphibians (terrestrial phase) and reptiles when no data are available. 

b

 Freshwater fish may be surrogates for amphibians (aquatic phase) when no data are available. 

Within each of these very broad taxonomic groups, an acute and/or chronic endpoint is 

selected from the available test data. A complete discussion of all toxicity data available for 

this risk assessment and the resulting measures of effect selected for each taxonomic group 

are included in Appendix E. 

1. Aquatic Effects 

Direct application of mandipropamid to streams, lakes, and ponds is prohibited by the 

product label. Immediately following application, the highest mandipropamid residue levels 

are expected to be located in surface waters adjacent to treated agricultural fields due to spray 

drift at the time of application and/or from runoff after a rain event. Mandipropamid may be 

transported off the field in runoff for several months after application. Exposure estimates 

for this screening level risk assessment focuses on the total residues for aquatic 

concentrations of the parent, mandipropamid, and its degradates of toxic concern 

SYN500003 and SYN504851. These degradates, which were identified in the suite of 

environmental fate studies, are according to the Health Effects Division, toxic degradates 

also found in residue studies. Fish, amphibians, and aquatic invertebrates that live in aquatic 

environments are potentially exposed to mandipropamid residues in surface water by direct 

contact of their integument (covering of the body or a part such as skin, gill membranes, 

cuticle, etc.) and via uptake through their gills or integument. Assessment endpoints were 

selected to assess reduced survival, growth, and reproduction in these taxonomic groups from 

combined direct contact with integument and uptake across the gill or integument. Because 

toxicity data for amphibians are rarely available, fish were used as a surrogate to assess risks 

to aquatic-stage amphibians (USEPA 2004). Aquatic plants are also potentially exposed by 

contact of their outer surface area with mandipropamid residues in surface water or through 

sorption and uptake through roots or across cell walls. 

Aquatic animals may also be exposed to mandipropamid residues in sediment or in their diet 

(i.e., detritus, aquatic plants, and/or prey). Sediment residues of mandipropamid and its 

degradates may potentially occur because of eroded soil in runoff depositing out to sediment 

and from the chemicals partitioning to sediment from water. Food chain transfer has the 

potential to occur where higher trophic level organisms feed on organisms that have taken up 

mandipropamid from surface water through their gills or integument or on organisms or 

detrital matter that have sorbed mandipropamid. No studies have been submitted regarding 

the potential for bioconcentration in aquatic organisms. Although the Koc values indicate that 
16

mandipropamid residues will partition to sediment to some degree, the log Kow of 3.13 

indicates that bioconcentration should not be of particular concern. 

Leaching (infiltration/percolation) may result in transport of mandipropamid through the soil 

column into ground water which may, in some circumstances, flow into a surface water 

body. The mobility of mandipropamid in soil is considered moderate based on batch 

adsorption experiments conducted in seven soils. 

2. Terrestrial Effects 

The highest mandipropamid residue levels are expected to be located in the surface soil and 

on foliage (e.g., short and tall grasses, broadleaf weeds), seeds, and insects on the treated 

agriculture field immediately following ground spraying. While spray drift may result in 

transport of mandipropamid to off-target field surface soil, foliage, and insects, the highest 

concentrations for these media are still expected to be those in the treated field. Birds, 

mammals, reptiles, and amphibians that ingest foliage, insects, and/or soil invertebrates from 

either the treated area or from spray drift impacted areas are potentially exposed to 

mandipropamid residues in their diet. Endpoints will be included that assess reduced 

survival, growth, and reproduction in these taxonomic groups from dietary exposure. 

Because toxicity data for reptiles and terrestrial-phase amphibians are rarely available, risk 

assessment results for birds will be used as surrogates to assess risks to reptiles and 

terrestrial-phase amphibians (USEPA 2004). 

Mandipropamid may reach off-field terrestrial or riparian/wetland vegetation environments 

in spray drift at the time of application. Following a rain event, mandipropamid may also 

reach off-field terrestrial or riparian/wetland vegetation environments in sheet and channel 

flow runoff. 

3. Ecosystems at Risk 

Ecosystems potentially at risk are expressed in terms of the selected assessment endpoints 

(Table 4). The typical assessment endpoints for screening-level pesticide ecological risks are 

reduced survival, and reproductive and growth impairment for both aquatic and terrestrial 

animal species. Aquatic animal species of potential concern include freshwater fish and 

invertebrates, estuarine/marine fish and invertebrates, and amphibians. Terrestrial animal 

species of potential concern include birds, mammals, and beneficial insects. For both aquatic 

and terrestrial animal species, direct acute and direct chronic exposures are considered. In 

order to protect threatened and endangered species, all assessment endpoints are measured at 

the individual level. Although endpoints are measured at the individual level, they provide 

insight about risks at higher levels of biological organization (e.g., populations and 

communities). For example, pesticide effects on individual survivorship have important 

implications for both population rates of increase and habitat carrying capacity. 

For terrestrial and semi-aquatic plants, the screening assessment endpoint is the perpetuation 

of populations of non-target species (crops and non-crop plant species). Existing testing 
17

requirements have the capacity to evaluate emergence of seedlings and vegetative vigor. 

Although it is recognized that the endpoints of seedling emergence and vegetative vigor may 

not address all terrestrial and semi-aquatic plant life cycle components, it is assumed that 

impacts at emergence and in active growth have the potential to impact individual 

competitive ability and reproductive success. For aquatic plants, the assessment endpoint is 

the maintenance and growth of standing crop or biomass. Measurements for this assessment 

endpoint focus on cell density, growth rates, and biomass in non-vascular plants (i.e., 

freshwater algae) and frond number, growth rate, and biomass in aquatic vascular plants 

(duckweed). 

The ecological relevance of selecting the above-mentioned assessment endpoints is as 

follows: (1) complete exposure pathways exist for these receptors; (2) the receptors may be 

potentially sensitive to pesticides in affected media and in residues on plants, seeds, and 

insects; and (3) the receptors could potentially inhabit areas where pesticides are applied, or 

areas where runoff and/or spray drift may impact the sites because suitable habitat is 

available. 

Table 4. Summary of Assessment Endpoints and Measures of Effect in Screening Level 

Risk Assessment 

Assessment Endpoint Measures of Effect 

1. Abundance (i.e., survival, reproduction, and 

growth) of individuals and populations of birds in 

close proximity to sites 

1a. Mallard duck (at least) acute oral LD50

1b. Mallard duck and bobwhite quail subacute 5-day 

dietary LC50

1c. Mallard duck (at least) reproduction NOAEL (e.g., 

number of eggs laid, set, cracked, etc.) 

2. Abundance (i.e., survival, reproduction, and 

growth) of individuals and populations of mammals in 

close proximity to sites 

2a. Laboratory rat (at least) acute oral (single dose) 

LD50

2b. Laboratory rat (at least) chronic (reproductive) 

NOAEC or NOAEL 

3. Survival and reproduction of individuals and 

communities of freshwater fish and invertebrates in 

close proximity to sites 

3a. Rainbow trout and bluegill sunfish (at least) acute 

96-hr LC50

3b. Rainbow trout or bluegill sunfish (preferred 

species tested that of the more acutely sensitive 

species tested) chronic early life-stage or life-cycle 

NOAEC (e.g., number hatched, time to hatch, 

mortality, growth of young) 

3c. Daphnia magna (at least) acute 48-hr EC50 (or 

96-hr LC50 for other invertebrates) where effect 

measured is surrogate for death 

3d. Daphnia magna (at least) chronic reproductive 

NOAEC (e.g., number of young produced, time to first 

brood release, parental survival, parental growth) 
18

Table 4. Summary of Assessment Endpoints and Measures of Effect in Screening Level 

Risk Assessment 

Assessment Endpoint Measures of Effect 

4. Survival and reproduction of individuals and 

communities of estuarine/marine fish and 

invertebrates in close proximity to sites 

4a. Atlantic silverside or sheepshead minnow (at least) 

acute 96-hr LC50

4b. Eastern oyster (at least) acute 96-hr EC50 where 

the effect measured is shell deposition or 

embryo/larval fertilization, survival, and normal shell 

development 

4c. Pink shrimp or mysid shrimp (at least) acute 96-hr 

LC50 or EC50 where the effect measured is a surrogate 

for mortality 

4d. Fish (prefer species that matches the most acutely 

sensitive fish tested) early life stage or life cycle 

NOAEC (e.g., number hatched, time to hatch, growth 

of young, overall survival) 

4e. Mysid shrimp (at least) chronic NOAEC 

5. Survival of beneficial insect populations in close 

proximity to sites 

1. Honey bee acute contact LD50

6. Survival and growth of terrestrial plants in close 

proximity to sites 

6a. Monocot and dicot seedling emergence EC25

6b. Monocot and dicot seedling emergence EC05 or 

NOAEC 

6c. Monocot and dicot vegetative vigor EC25

6d. Monocot and dicot vegetative vigor EC05 or 

NOAEC 

7. Standing crop or biomass and growth of aquatic 

plants in close proximity to sites 

7a. Green and blue-green alga (at least) EC50

7b. Freshwater and saltwater diatom and duckweed (at 

least duckweed) acute EC50

7c. Green and blue-green algae, a freshwater and 

saltwater diatom and duckweed (at least) EC05 or 

NOAEC 

LD50 = Lethal dose to 50% of the test population. 

LC50 = Lethal concentration to 50% of the test population. 

EC50/EC25/EC05= Effect concentration to 50/25/5% of the test population. 

IC25/IC05 = 25/5% Inhibitory concentration. 

NOAEC = No observed adverse effect level. 

LOAEC = Lowest observed adverse effect level. 
19

C. Assessment Endpoints 

Assessment endpoints are defined as “explicit expressions of the actual environmental value 

that is to be protected”. Defining an assessment endpoint involves two steps: (1) identifying 

the valued attributes of the environment that are considered to be at risk; and (2) 

operationally defining the assessment endpoint in terms of an ecological entity (i.e., a 

community of fish and aquatic invertebrates) and its attributes (i.e., survival and 

reproduction). Therefore, selection of the assessment endpoints is based on valued entities 

(i.e., ecological receptors), the ecosystems potentially at risk, the migration pathways of 

pesticides, and the routes by which ecological receptors are exposed to pesticides. The 

selection of clearly defined assessment endpoints is important because they provide direction 

and boundaries in the risk assessment for addressing risk management issues of concern. 

This ecological risk assessment considers maximum application rates of mandipropamid to 

fields that have vulnerable soils, maximum number of applications, and minimum intervals 

for uses on representative crops grown on runoff prone soils to estimate exposure 

concentrations. In addition, this assessment is not intended to represent a site- or timespecific analysis. Instead, this assessment is intended to represent high-end exposures at a 

national level. Likewise, the most sensitive toxicity measures of effect are used from 

surrogate test species to estimate treatment-related direct effects on acute mortality and 

chronic reproductive, growth, and survival assessment endpoints. Toxicity tests are intended 

to determine effects of mandipropamid exposure on birds, mammals, fish, terrestrial and 

aquatic invertebrates, and plants. These tests include short-term acute, subacute, and 

reproductive studies and are typically arranged in a hierarchical or tiered system that 

progresses from basic laboratory tests to applied field studies. The toxicity studies are used to 

evaluate the potential of mandipropamid to cause adverse effects, to determine whether 

further testing is required, and to determine the need for precautionary label statements to 

minimize the potential adverse effects to non-target animals and plants (CFR 40 §158.202, 

2002a). A summary of measures of effects selected to characterize potential ecological risks 

associated with exposure to mandipropamid is provided in Table 4. 

D. Conceptual Model 

In order for a chemical to pose an ecological risk, it must reach ecological receptors in 

biologically significant concentrations. An exposure pathway is the means by which a 

contaminant moves in the environment from a source to an ecological receptor. For an 

ecological exposure pathway to be complete, it must have a source, a release mechanism, an 

environmental transport medium, a point of exposure for ecological receptors, and a feasible 

route of exposure. In addition, the potential mechanisms of transformation (i.e., which 

degradates may form in the environment, in which media, and how much) must be known, 

especially for a chemical whose metabolites/degradates are of greater toxicological concern. 

In this assessment the parent, mandipropamid, and its degradates of toxic concern, 

SYN500003 and SYN504851 (as identified by HED) are quantitatively assessed together as 

total residues of mandipropamid. The assessment of ecological exposure pathways includes 

an examination of the source and potential migration pathways for constituents, and the 
20

determination of potential exposure routes (e.g., ingestion, inhalation, and dermal 

absorption). 

1. Risk Hypotheses 

Risk hypotheses are specific assumptions about potential adverse effects (i.e., changes in 

assessment endpoints) and may be based on theory and logic, empirical data, mathematical 

models, or probability models (USEPA 2004). For this assessment, the risk is stressorinitiated, where the stressor is the release of mandipropamid to the environment. The 

following risk hypothesis is presumed for this screening level assessment:

The use of mandipropamid as an fungicide in agricultural settings on field brassica 

vegetables, bulb vegetables, cucurbits, fruiting vegetables, grapes, leafy vegetables, 

potatoes, tomatoes, tuberous and corm vegetables involves situations where terrestrial 

and/or aquatic animals and plants may be exposed to the chemical. Based on information 

on persistence, mode of action, direct toxicity and potential indirect effects to trophic 

food webs, EFED assumes that mandipropamid together with its degradates of concern, 

SYN500003 and SYN504851 have the potential to cause reduced survival and 

reproductive impairment to terrestrial and aquatic animals and plants.

2. Diagram 

The source and mechanisms of release of mandipropamid are ground and aerial application 

to agricultural crops. The conceptual model and subsequent analysis of exposure and effects 

are all based on mandipropamid and its degradates of concern, SYN500003 and SYN504851. 

Surface water runoff from the areas of application is assumed to follow topography. 

Additional release mechanisms include spray drift and wind erosion, which may potentially 

transport contaminants into the air. Potential emission of volatile compounds is not 

considered as a viable release mechanism for mandipropamid, because vapor pressure 

information suggests that volatilization is not expected to be a significant route of dissipation. 

The conceptual model shown in Figure 2 depicts the potential source, release mechanisms, 

abiotic receiving media, and biological receptor types. 
21

Figure 2. Conceptual Model Depicting Ecological Risk Based on the Proposed 

Mandipropamid Application

Stressor Application of Mandipropamide, to Any of Its Proposed Use Crops

Source:

Transport 

Pathway Direct Ground Deposition Spray Drift Volatilization Wind Suspension Runoff/

Erosion Leaching

Source:

Exposure 

Media Terrestrial Food

Residues (foliage, fruit,

Insects;) 

Upland Soil

And Foliage

Riparian/Wetland

Foliage/Soil

Surface Water

Sediment Groundwater

Exposure Point

Direct Contact

And Ingestion

Direct Contact/

Root Uptake

Uptake/Adsorption Gill/Integument Uptake

Receptors

Terrestrial Vertebrates and 

Invertebrates

Terrestrial Upland

Plants

Riparian/Wetland 

Plants Aquatic Plants Aquatic Invert and Vertebrates

Direct Effects

Terrestrial Animal

•Lethality

•Reproductive/

developmental 

Effects

•Other adverse 

sublethal effects

Non-Target Plants

•Plant growth abnormalities

•Lethality

•Developmental/reproductive

effects

Plant Population

Reduced Population

growth

Aquatic Animals and Plants

•Effects to survival, growth, and 

Reproduction

•Reproduction in cell density/biomass 

in aquatic plants

• Other adverse sublethal effects

Indirect 

Effects

Altered Terrestrial Community Assemblages:

Reduced food supply and edge habitat availability

Altered Aquatic Community Assemblages:

Effects to riparian habitat availability

Effects to 

E. Analysis Plan 

1. Preliminary Identification of Data Gaps and Methods 

Based on EFED’s review of the currently available data, the identified data gaps are as 

follows: 

• acceptable fish acute toxicity data (current studies are invalid) 

• acceptable invertebrate chronic toxicity data (current studies are invalid) 

2. Measures to Evaluate Risk Hypotheses and Conceptual Model 

a. Measures of Exposure 

The proposed uses for mandipropamid are for brassica vegetables, bulb vegetables, cucurbits, 

fruiting vegetables, grapes, leafy vegetables, potatoes, tomatoes, tuberous and corm 

vegetables. Since mandipropamid is currently not registered for use on these crops, no 
22

statistics exist regarding the amount of mandipropamid that has been applied to these crops in 

the past. However, the present geographic distribution for these proposed site uses are 

expected to generally represent potential mandipropamid application areas. 

For agricultural uses, exposure concentrations for aquatic ecosystem assessments will be 

estimated based on EFED’s aquatic Tier I model GENEEC. Among the major degradates 

identified in various fate studies (CGA380778, NOA458422, CGA380775, SYN500003, 

SYN536638, and SYN504851), only SYN500003 and SYN504851 were identified by the 

Office of Pesticides Programs Human Health Effects Division (HED) to be of toxic concern. 

There are no available ecotoxicity data for these two degradates. This assessment will 

assume that these degradates have similar toxicity as the parent. Total residue data were used 

in EFED’s aquatic Tier I model GENEEC. 

Residues in potential dietary sources (e.g., vegetation and insects) for mammals and birds 

will be estimated using the Tier I model T-REX Version 1.3.1 (USEPA 2006a). This model 

provides estimates of concentrations (maximum, or upper bound, and average) of chemical 

residues on the surfaces of different types of foliage that may be sources of dietary exposure 

to avian, mammalian, reptilian, or terrestrial-phase amphibian receptors. The surface residue 

concentration (ppm) is estimated by multiplying the application rate (pounds active 

ingredient per acre) by a value specific to each food item. For both mammals and birds, 

three animal body weight classes are considered. The T-REX model will be run using the 

maximum application rate for all proposes uses (which is 4 applications of 0.13 lbs a.i./acre 

with a minimum of 7 days between each application). 

Exposure to terrestrial and semi-aquatic (wetland) plants will be estimated using the 

TerrPlant model Version 1.2.2 (USEPA 2006b). The TerrPlant model estimates risk quotients 

for non-target monocot and dicot plants that may be exposed to pesticides applications via 

runoff and/or spray drift to terrestrial plants inhabiting dry and semi-aquatic (wetland) areas. 

RQs are calculated using the EC25 value for non-threatened/endangered plants and the EC05

or NOAEC value for threatened/endangered plants. 

b. Measures of Effect 

Measures of ecological effects are obtained from a suite of registrant-submitted guideline 

studies conducted with a limited number of surrogate species. Registrant-submitted data 

suitable for quantitative risk assessment are available for acute exposure of birds, terrestrial 

invertebrates, freshwater and marine/estuarine invertebrate, and terrestrial plants, and for 

chronic exposure to birds, mammals, and freshwater fish. A generic summary of the 

measures of effect based on pesticide toxicity studies for different ecological receptors and 

effect endpoints (acute/chronic) is given in Table 4. 

c. Measures of Ecosystem and Receptor Characteristics 

For the assessments using the Tier I aquatic model GENEEC and the Tier I terrestrial models 

T-REX and TerrPlant, the ecosystems that are modeled are intended to be generally 
23

representative of any aquatic or terrestrial ecosystem associated with areas where 

mandipropamid could be used. For aquatic assessments, fish and aquatic invertebrates in 

both freshwater and estuarine/marine environments are represented, as well as aquatic plants. 

For terrestrial assessments, three different size classes of small birds and mammals are 

represented, along with four potential foraging categories, as well as two terrestrial plant 

groups (upland plants and plants growing in semi-aquatic areas). 
24

III. ANALYSIS 

A. Use Characterization 

The purpose of the ecological risk assessment is to assist the Agency in evaluating the 

actions needed, if any, to address ecological risks associated with uses of the new fungicide, 

RevusTM (proposed name mandipropamid), for use on brassica vegetables, bulb vegetables, 

cucurbits, fruiting vegetables, grapes, leafy vegetables, potatoes, tomatoes, tuberous and 

corm vegetables. This chemical is to be applied on commercial or farm plantings via ground 

or aerial applications. It requires the use of an external adjuvant (such as a non-ionic 

surfactant, crop oil concentrate, silicone based, or blend) to enhance fungicidal activity. 

Mandipropamid is a new chemical, currently unregistered for use. Therefore, there is no 

current chemical usage information available in the National Center for Food and 

Agricultural Policy (NCFAP) pesticide use database or the U.S. Department of Agriculture 

National Agriculture Statistics Service (NASS) chemical use database. 

The proposed label specifies that mandipropamid is intended for the control of foliar 

oomycete pathogens in a range of crops including Plasmopara viticola in grapes, 

Phytophthora infestans in potatoes and tomatoes and Pseudoperonospora cubensis in 

cucurbits 

The proposed label specifies that the maximum amount of the active ingredient that may be 

applied in a single growing season is 0.52 lbs a.i./acre. According to the proposed label, this 

application amount may be divided into 4 applications of 0.13 lbs a.i./acre with 7 day 

intervals between each application. 

Product information:

Product Name: Mandipropamid Fungicide (proposed name RevusTM) 

Active Ingredients: 

Mandipropamid....................................................................................................................... 23.3% 

Inert ingredients ...................................................................................................................... 76.7% 

Total ......................................................................................................................................... 100% 

(CAS Number 374726-62-2) 
25

Table 5. Application Rates of Mandipropamid 

Crops 

Disease 

Control 

Application 

Rate 

(lbs a.i./acre) 

Maximum 

No. 

Applications 

per Season Interval Restrictions 

Brassica 

vegetables, 

bulb vegetables, 

cucurbits, 

fruiting 

vegetables, 

grapes, 

leafy 

vegetables, 

potatoes, 

tomatoes, 

tuberous and 

corm vegetables 

foliar oomycete 

pathogens in a 

range of crops 

including 

Plasmopara 

viticola 

in 

grapes, 

Phytophthora 

infestans

0.13 4 7-day minimum 

interval 

between 

applications 

Do not apply: 

1. More than 32 

fl oz of product 

/A/Season 

2. Within 1 day 

of harvest for 

brassica, leafy 

vegetables, 

fruiting 

vegetables, 

tomatoes. 

3. Within 7 days 

of harvest for 

bulb vegetables. 

4. Within 14 

days of harvest 

for potatoes, 

grapes 

B. Exposure Characterization 

1. Environmental Fate and Transport Characterization 

Data were submitted regarding the hydrolysis, photolysis, biodegradation, soil adsorption 

properties, and field dissipation of mandipropamid. These data are sufficient to characterize 

the transport, partitioning, mobility, and degradation of mandipropamid and several of its 

major metabolites in the environment. The physical and chemical properties used to 

characterize the environmental fate of mandipropamid were summarized in Table 2. 

Chemical names and structures of the metabolites discussed below are provided in Appendix 

A. 

a. Summary of Empirical Data 

Registrant submitted studies indicate that mandipropamid is persistent in the environment, 

under aerobic aquatic conditions. Mandipropamid appears to be stable to hydrolysis at 

environmental pH (pH range 5–9) but susceptible to photolysis in soil and water. Due to its 

vapor pressure and Henry’s Law constant, volatilization from water and soil is not expected 

to be an important environmental fate process. Mandipropamid and several of its metabolites 

can be mobile in soil and have the potential to leach into ground water. 
26

b. Degradation and Metabolism 

Mandipropamid did not undergo abiotic hydrolysis in pH 5, 7, and 9 aqueous buffered 

solutions maintained at 25 °C over the course of a 30 day incubation period (MRID 

46800007&8). The environmental photolysis half-lives of mandipropamid in pH 7, 25°C 

aqueous solution were estimated as 0.63-1.1 days (MRID# 46800009,10,13,14). The soil 

photolysis half-lives of mandipropamid were estimated as 16.4–23.9 days (MRID

46800015,16,17). 

The linear biodegradation half-life of mandipropamid in six European and one U.S. soils 

ranged from approximately 26 to 103 days under aerobic conditions (MRIDs 

46800020,21,22,24-28). 

Based on results form a supplemental study, under anaerobic conditions the rate of 

biodegradation appears to be much slower. Mandipropamid degraded with linear half-lives of 

151 days in a silt loam soil from Switzerland maintained under anaerobic conditions (MRID 

48600022). 

The aerobic aquatic degradation half-lives of mandipropamid were 17.8-18.5 days in two 

river water/silt loam sediment systems from England Germany (MRID 46800030-31). 

The degradation of one mandipropamid metabolites was studied in three soils under aerobic 

conditions, and this metabolite appears to be non-persistent. Based on linear regression 

analysis, the half-lives of CGA380778 in silt loam soil from Switzerland, a sandy clay loam 

soil from England, and sandy loam soil from US, were 6.4, 6.9, and 58 days, respectively 

(MRID# 46800023). 

c. Transport and Mobility 

Volatilization of mandipropamid from treated fields and water surfaces is not expected to be 

an important environmental fate process based on a Henry’s Law constant of 8.29x10-9 atmm3

/mol, and vapor pressure of 3.52x10-8 mm Hg (MRID# 46800007, 8). 

Mandipropamid is expected to possess moderate mobility in soils based upon Koc values 

ranging from 405 - 1294, measured in seven soils from the U.S. and Europe (MRID 

46800038-41). Given the range of Koc values in the six soils tested, mandipropamid 

possesses the potential to leach into ground water. 

The mobility of mandipropamid metabolites SYN52119, SYN500003, CGA380778, and 

SYN504851 were also studied. All of these metabolites are expected to possess high 

mobility in soils based upon the submitted data and have the potential to leach into ground 

water. Koc values of <1 to 31 L/kg were observed in 12 soils (MRID# 46800035, 36, 42-44). 
27

d. Field Studies 

Terrestrial field dissipation studies (MRID 46800045-47) for mandipropamid were studied in 

four bare plots cropped with field potatoes: in California (sandy loam soil), New York 

(loamy sand soil), and Georgia (sandy loam soil). 

The field dissipation half-lives of mandipropamid were: 75.3 days (California site); 100.5 

days (New York); 81.5 days (Georgia). 

At the California, residues of mandipropamid and CGA380778 were only detected in the top 

15 cm of the soil. 

At the New York site, residues of mandipropamid and CGA380778 were only detected in the 

top 15 cm of the soil. 

At the Georgia site, residues of mandipropamid and CGA380778 were only detected in the 

top 15 cm of the soil with one exception; mandipropamid was detected once in the 15-30 cm 

depth at 14 days post-treatment. 

2. Measures of Exposure 

a. Aquatic Exposure Modeling 

Exposure concentrations of mandipropamid together with its degradates of concern 

(SYN500003 and SYN504851) were estimated based on the EFED aquatic Tier I model 

GENEEC 2.0 (see Appendix B for explanation of model). 

The aquatic exposure modeling inputs and outputs for mandipropamid including its 

degradates, SYN500003 and SYN504851, are shown in Tables 6 and 7. 

Table 6. GENEEC Chemical Specific Input Parameters for mandipropamid and its degradate, 

SYN500003 and SYN504851. 

Parameter Input Value and Unit Source 

Maximum application rate 0.13 lb a.i./A Product Label EPA Reg. No. 100-RELU.

Maximum number of applications 4 Product Label EPA Reg. No. 100-RELU.

Method of Aerial Product Label EPA Reg. No. 100-RELU.

Minimum interval between 

applications 

7 days Product Label EPA Reg. No. 100-RELU.

Partition coefficient Koc 2.89 mL/g For SYN500003; Lowest non-sand Koc; MRID 

46800042,43 

Aerobic soil metabolism 72.04 days Total toxic of parent and degradates; MRID 

46800021. Input Parameters Guidance, 2002 
28

Table 6. GENEEC Chemical Specific Input Parameters for mandipropamid and its degradate, 

SYN500003 and SYN504851. 

Parameter Input Value and Unit Source 

Aerobic aquatic metabolism (t1/2) 102 days Total toxic of parent and degradates; MRID 

46800030-31. Input Parameters Guidance, 

2002 

Aquatic photolysis t1/2 (days) 1.1 For parent; MRID 46800014; input Parameters 

Guidance, 2002 

Table 7. GENEEC2 Model Estimated Environmental Concentrations (EEC) of 

mandipropamid and its degradates identified as of toxicological concerns, in standard farm 

pond. 

Compound Peak (ppb) 4-day (ppb) 21-day (ppb) 60-day 

(ppb)

90-day 

(ppb)

Total 

Residue 

including 

mandipropamid 

and 

its degradates, 

SYN500003 and 

SYN504851 

20.9 20.7 19.4 16.9 15.3 

b. Aquatic Exposure Monitoring and Field Data 

Since mandipropamid is a new use chemical that has not been registered, no monitoring data 

exist at this time. 

3. Measures of Terrestrial Exposures 

a. Terrestrial Exposure Modeling 

The EFED terrestrial exposure model T-REX (T-REX, version 1.3.1) is used to estimate 

exposures and risks to avian and mammalian species. The model provides estimates of 

exposure concentrations and risk quotients (RQs). Specifically, the model provides estimates 

of concentrations (maximum, or upper bound, and average, or mean) of chemical residues on 

the surface of different types of foliage and insects that may be dietary sources of exposure to 

terrestrial wildlife receptors. 
29

T-REX was run for the proposed new uses of mandipropamid using the input values provided 

in Table 8. Potential risk from mandipropamid and its degradates were addressed by using 

the default half-life of 35 days which operationally results in mandipropamid being relatively 

stable and is comparable to a total residue approach where the degradates are assumed to be 

as toxic as the parent. The maximum label rate selected for modeling is the same maximum 

label rate for all proposed uses. 
30

Table 8. Input Parameters Used in T-REX Version 1.3.1 to Determine Terrestrial EECs for 

Mandipropamid Application on all proposed uses. 

Input Variable Parameter Value Source 

Maximum application rate 0.13 Product label 

Maximum number of 

applications per year 

4 Product label 

Minimum application interval 7 Product label 

Foliar half-life 35 Default value 

Mineau et al. scaling factor 1.15 Default value 

Application type Ground Spray 

or Aerial Spray 

Product label 

Avian 

acute 

oral toxicity 

No input 

value 

because 

mandipropamid is 

practically nontoxic 

to birds on an acute oral 

basis (No mortalities in 

acute oral test) 

468001-10

Avian 

acute 

dietary 

toxicity 

No 

input 

value 

because 

mandipropamid 

practically nontoxic 

to birds on an acute 

dietary basis 

(No mortalities 

in acute dietary test ) 

468001-12

Avian 

reproductive 

toxicity: 

NOAEC = 1060 467152-14 

Mammalian 

Acute 

Oral LD50 1

No 

input 

value 

because 

mandipropamid 

practically nontoxic 

to mammals on an 

acute 

dietary basis 

(No mortalities 

in acute dietary test ) 

46800202 

Toxicity values 

Mammalian 

Reproductive 

Toxicity 

NOAEC = 

250 ppm 

46800230 

A summary of the terrestrial animal estimated exposure concentrations (EECs) in forage 

generated by T-REX is presented in Table 9. Mandipropamid residues (ppm) ranged from 6 
31

ppm (fruits/pods/large insects) to 103 ppm (short grass) for maximum residues and 3 ppm 

(fruits/pods/large insects) to 36 ppm (short grass) for mean residues. 

Table 9. Peak Terrestrial EECs Estimated Using Kenaga Values for 

Mandipropamid Applied to all the proposed uses 

Forage Type Maximum Residue 

(ppm) 

Mean Residue (ppm) 

Short grass 103 36 

Tall grass 47 15 

Broadleaf plants and small insects 58 19 

Fruits/pods/large insects 6 3 

TerrPlant (TerrPlant, version 1.2.2, dated December 26, 2006) was used to estimate 

exposures and risks to terrestrial plant species. Input parameters for the model included: (1) 

toxicity values for monocots and dicots; (2) application rate; (3) runoff, based on chemical 

solubility; and (4) soil incorporation depth. The model provides estimates of exposure 

concentrations and risk quotients (RQs) for non-listed and listed terrestrial and semi-aquatic 

plants. Input and output values used for estimating terrestrial and semi-aquatic plant exposure 

risks to mandipropamid are summarized in Tables 10 and 11, respectively. Only one 

application is considered in this assessment due to model limitations. More detailed 

information on TerrPlant Version 1.2.2 is presented in Appendix D. 

Table 10. Input Parameters Used in TerrPlant 1.2.2 to Determine Terrestrial EECs for Plants 

for Mandipropamid Application on all proposed Crops based on the maximum proposed 

application rate. 

Input Variable Parameter Value Source 

Maximum application rate 0.13 lbs a.i./acre Product label 

Runoff value (0.01, 0.02, or 0.05 if 

chemical solubility <10, 10–100, or >100 

ppm, respectively) 

0.02 * MRID 46800009 

Minimum incorporation depth (inches) 0 Product label 

Toxicity Values Most Sensitive Vegetative Vigor Endpoint 

Values 

EC25 >0.792 

NOAEC = 0.198 lbs a.i./acre 

Most Sensitive Seedling Emergence 

Endpoint Values 

EC25 > 

NOAEC = 0.165 lbs a.i./acre 

MRID 46695512 

a

 Based on the water solubility of 2.3 ppm. 
32

Table 11. Summary Output EECS from TerrPlant for Mandipropamid 

Application Method 

EECs for Plants 

Inhabiting Areas 

Adjacent to 

Treatment Site 

(lbs a.i./acre), 

Run off & Drift Load 

EECs for SemiAquatic Plants 

Inhabiting Areas 

Adjacent to 

Treatment Site (lbs 

a.i./acre), 

Run off & Drift Load 

Drift EEC 

(lbs a.i./acre) 

Ground spray 

(unincorporated) 

0.0039 0.0273 0.0013 

Aerial 0.0091 0.0325 0.0065 

b. Terrestrial Residue Studies 

No residues studies were submitted for any of the proposed new uses. 

C. Ecological Effects Characterization 

In screening-level ecological risk assessments, the effects characterization describes the types 

of effects a pesticide can have on aquatic or terrestrial organisms. This characterization is 

based on registrant-submitted studies that describe information regarding acute and chronic 

toxicity effects of mandipropamid (Technical Grade Active Ingredient (TGAI)) for various 

aquatic and terrestrial animals. Also included in this characterization is a limited set of 

aquatic organism studies testing the toxicity of the mandipropamid degradate, CGA380778. 

Appendix E summarizes the results of all registrant-submitted toxicity studies used to 

characterize effects for this risk assessment. 

1. Aquatic Effects Characterization 

The most sensitive freshwater and estuarine/marine acute and chronic toxicity values for 

mandipropamid and its degradate, CGA380778, are summarized in Tables 12 and 13. 

Toxicity values typically used by EFED to assess a pesticide’s acute risk to fish were not 

available. This is because all fish acute toxicity studies were deemed invalid. Although 

aquatic organism results were limited, a Daphnia magna, water flea, acute toxicity test was 

available for both the parent (48-h 7.1 ppm a.i.) and degradate (48-h 54.2 ppm). As the 

degradate was less toxic than the parent, the measures of toxicity used to evaluate risks to 

aquatic organisms were based solely on the parent toxicity data (Table 15). 
33

Table 12. Mandipropamid Values Used to Calculate Screening Level Risks to Aquatic 

Organisms and Aquatic Plants 

Selected Test and Measurement Endpoint Assessment 

Endpoint(a)

Measures of 

Effect(a) Species Toxicity 

Value 

Study 

Conditions

Basis for 

selection 

Reference 

(Classification) 

3a. freshwater 

fish acute 96-hr 

LC50

No acceptable 

studies b

-- -- -- -- 

3c. Freshwater 

invertebrate 

acute 96-h LC50

(for copepods 

48-h LC50 or 

EC50 where the 

effect measured 

is surrogate) 

Water flea (Dapnia 

magna) 

<24 hours old 

48-h EC50

= 7.1 ppm 

a.i. 

(effects: 

immobility 

and 

mortality) 

TGAI 

96.5% a.i., 

pH range of 

7.93-8.07, 

Temperature 

range of 

20O + 1OC 

Hardness 

range of 

226 mg as 

CaCO3/L 

Most 

sensitive 

(only a 

single 

TGAI test) 

MRID 468000-50 

(Acceptable) 

Survival and 

reproduction of 

individuals and 

communities of 

freshwater fish 

and 

invertebrates in 

close proximity 

to sites 

3d. Freshwater 

invertebrate 

reproductive 

NOAEC 

No acceptable 

studies 

-- -- -- -- 

4a. Estuarine or 

marine fish 

acute 96-hr 

LC50

No acceptable study -- -- -- -- 

4b. Mollusc 

acute 96-hr 

EC50 shell 

deposition 

Eastern oyster 

(Crassostrea 

virginica) 

96-h EC50

= 0.91 ppm 

a.i. 

TGAI 96.1 

% a.i., pH 

range of 

8.1- 8.3, 

Temperature 

range of 

19.1-

19.7OC, 

Most 

sensitive 

(only a 

single test 

result) 

MRID 468001-01 

(Acceptable) 

Survival and 

reproduction of 

individuals and 

communities of 

estuarine/marine 

fish and 

invertebrates in 

close proximity 

to sites 

4c. Shrimp 

acute 96-hr 

LC50

Mysid shrimp 

(Americamysis 

bahia) 

96-h LC50 

= 1.7 ppm 

a.i. 

TGAI 

96.1% a.i., 

pH range of 

8.1-8.4, pH 

7.5 + 1, 

Temperature 

range 23OC26O

Most 

sensitive 

(only a 

single test 

result) 

MRID 468001-02 

(Acceptable) 
34

Table 12. Mandipropamid Values Used to Calculate Screening Level Risks to Aquatic 

Organisms and Aquatic Plants 

Selected Test and Measurement Endpoint Assessment 

Endpoint(a)

Measures of 

Effect(a) Species Toxicity 

Value 

Study 

Conditions

Basis for 

selection 

Reference 

(Classification) 

4d. Fish early 

life stage or full 

life cycle 

NOAEC 

Fathead minnow 

(Pimephales 

promelas) 

NOAEC = 

0.22 ppm 

LOAEC = 

0.47 ppm 

TGAI 

96.5% a.i., 

Hardness 

range of 

38.3-58.0 

mg/L as 

CaCO3

pH: 7.1-7.9 

Temperature 

range of 

24.0-25.5°C

Most 

sensitive 

endpoint 

produced in 

the only 

fish chronic 

toxicity test 

available 

MRID 468001-08 

(Acceptable) 

4e. Invertebrate 

life cycle 

NOAEC 

No data submitted -- -- -- -- 
35

Table 12. Mandipropamid Values Used to Calculate Screening Level Risks to Aquatic 

Organisms and Aquatic Plants 

Selected Test and Measurement Endpoint Assessment 

Endpoint(a)

Measures of 

Effect(a) Species Toxicity 

Value 

Study 

Conditions

Basis for 

selection 

Reference 

(Classification) 

7a. Freshwater 

green algae, 

cyanobacteria 

or diatom 96-h 

EC50 for 

biomass 

Green algae 

(Pseudokirchneriella 

subcapitata)

96-h EC50

>2.5 ppm 

TGAI 

96.5%, 

static, 

temperature 

range of 24 -

25OC 

Most 

sensitive 

endpoint 

(Only 

nonvascular 

aquatic 

plant 

endpoint 

available) 

MRID 468001-21 

(Acceptable) 

7b. Saltwater 

green algae or 

diatom 96-h 

EC50 for 

biomass 

No submitted studies -- -- -- -- 

7c. Vascular 

plant (at least 

duckweed) 7- to 

14-d EC50 for 

biomass 

Duck weed 

(Lemna Gibba G3) 

96-h EC50

> 7.9 ppm 

TGAI 

96.1%, 

static 

renewal, pH 

of 7.5 

temperature 

range of 

24.5-24.9o

C,

Most 

sensitive 

(Only 

vascular 

aquatic 

plant 

endpoint 

available) 

MRID 468001-19 

(Acceptable) 

7d. Freshwater 

green algae, 

cyanobacteria 

or diatom 96-h 

NOAEC (or 

EC05) for 

biomass 

Green algae 

(Pseudokirchneriella 

subcapitata)

96-h EC50

NOAEC 

= 1.3 ppm 

TGAI 

96.5%, 

static, 

temperature 

range of 24 -

25OC 

Most 

sensitive 

endpoint 

(Only 

nonvascular 

aquatic 

plant 

endpoint 

available) 

MRID 468001-21 

(Acceptable) 

Standing crop 

or biomass and 

growth of 

aquatic plants in 

close proximity 

to sites 

7e.Vascular 

plant (at least 

duckweed) 7- to 

14-d NOAEC 

(or EC05) for 

biomass 

Duck weed 

(Lemna Gibba G3) 

96-h IC05

= 1.3 ppm 

TGAI 

96.1%, 

static 

renewal, pH 

of 7.5 

temperature 

range of 

24.5-24.9o

C,

Most 

sensitive 

(Only 

vascular 

aquatic 

plant 

endpoint 

available) 

MRID 468001-19 

(Acceptable) 

(a) Assessment endpoints and measures of effect identified to be assessed in the problem formulation (Table 4). 

(b) Fish acute toxicity is currently unavailable because the submitted fish acute toxicity studies were deemed 

invalid 
36

Table 13. Mandipropamid degradate, CGA380778, Aquatic Organism and Aquatic Plant 

Toxicity Values 

Test and Measurement Endpoints 

Assessment 

Endpoint 

Measures of 

Effect Species 

Toxicity 

Value 

Study 

Conditions 

Basis 

for 

selection 

Reference 

(Classification)

3a. Freshwater 

fish acute 96-hr 

LC50

Survival and No acceptable study -- -- -- -- 

reproduction of 

individuals and 

communities of 

freshwater fish 

and 

invertebrates in 

close proximity 

to sites 

3c. Freshwater 

invertebrate 

acute 96-h LC50

(for copepods 

48-h LC50 or 

EC50 where the 

effect measured 

is surrogate) 

Water flea (Dapnia 

magna) 

<24 hours old 

48-h EC50

= 54.2 

ppm a.i. 

(effects: 

immobility 

and 

mortality) 

98% purity, 

static, pH range 

of 7.9-

8.0,Temperature

range of 

20+1OC, 

Hardness of 219 

mg as CaCO3/L,

-- MRID 468000-

51 

(Acceptable) 

7a. Freshwater 

green algae, 

cyanobacteria or 

diatom 96-h 

EC50 for 

biomass 

Pseudokirchneriella 

subcapitata 

(Freshwater green 

algae) 

96-h 

EC50 = 16 

ppm a.i. 

98% purity, 

static, pH range 

7.4 – 10, 

Temperature 

range of 23.8-

24.3o

C 

Standing crop -- -- 

or biomass and 

growth of 

aquatic plants 

in close 

proximity to 

sites 

7d. Freshwater 

green algae, 

cyanobacteria or 

diatom 96-h 

NOAEC (or 

EC05) for 

biomass 

Pseudokirchneriella 

subcapitata 

(Freshwater green 

algae) 

96-h 

NOAEC = 

2.4 ppm 

-- -- -- 

a. Aquatic Animals 

(1). Acute Effects 

Freshwater Fish

At a minimum two freshwater fish acute toxicity studies using the TGAI are required to 

establish the toxicity of mandipropamid to fish. The preferred test species are rainbow trout 

(a coldwater fish) and bluegill sunfish (a warmwater fish). The registrant submitted three 

freshwater fish toxicity studies including two studies testing mandipropamid (TGAI; MRID’s 

468001-05, and MRID 468001-06) and one study testing the degradate CGA380778 (MRID 

468001-04). All of the studies were deemed invalid because of significant deviations from 

the guidelines. The studies were invalidated because the dissolved mandipropamid 

concentration was not determined (test solutions contained undissolved particulate test 

material and the measured concentrations were significantly unstable throughout the testing). 
37

Therefore, it is not possible to obtain accurate toxicity endpoint values that could be used for 

risk assessment purposes. 

Freshwater Invertebrates

A freshwater aquatic invertebrate toxicity test using the TGAI is required to establish the 

toxicity of mandipropamid to aquatic invertebrates. The preferred test species is Daphnia 

magna. Two freshwater invertebrate toxicity studies, one testing mandipropamid (TGAI), 

and the other testing the mandipropamid degradate, CGA38077, (MRID’s 468001-50 and 

468001-51, respectively) were submitted by the registrant. Both studies were classified as 

scientifically sound and acceptable for assessing risks to freshwater invertebrates; Guideline 

§72-2 (draft OPPTS 850.1010) is fulfilled. Since the 48-h EC50 (7.1 ppm a.i.) for 

mandipropamid falls in the range of 1 - 10 ppm, mandipropamid is classified as moderately 

toxic to aquatic invertebrates on an acute basis. Since the 48-h EC50 (54.2 ppm) for the 

major degradate of mandipropamid, CGA380778 falls in the range of 10 – 100 ppm, 

CGA380778 is classified as practically nontoxic to freshwater invertebrates. The more 

sensitive value of the parent was selected for use in assessing risk to freshwater invertebrates 

(Table 12). 

Estuarine/Marine Fish

Mandipropamid usage may occur in some areas associated with marine/estuarine habitats. 

Thus, marine/estuarine fish toxicity data is required (40CFR Part 158) to assess acute risks 

from mandipropamid use. Two marine/estuarine fish studies testing mandipropamid were 

submitted by the registrant (MRID 468001-03 and –05). However both studies were 

reviewed and identified as scientifically unsound because of significant deviations from the 

850 guidelines. The studies were invalidated because test solutions contained undissolved 

particulate test material, and the mean measured concentrations were significantly unstable 

throughout the test. Hence, no scientifically sound dissolved endpoint value can be 

determined for these studies. The 40CFR Part 158 acute marine/estuarine fish test 

requirement (Guideline §72-1, draft OPPTS 850.1075) is not fulfilled. 

Estuarine/Marine Invertebrates

Mandipropamid usage may occur in some areas associated with marine/estuarine habitats. 

Thus, marine/estuarine invertebrate toxicity data for a mollusk (shell deposition or embryolarval test), and shrimp is required (40CFR Part 158) to assess acute risks from 

mandipropamid use. The registrant submitted two marine/estuarine invertebrate toxicity 

studies testing mandipropamid (MRID’s 468001-02 and 468001-01). One study tested the 

acute toxic effect of manipropamid on mysid shrimp mortality and the other study tested 

mandipropamid’s acute toxic effects on shell deposition of the eastern oyster. Both tests 

were reviewed and found to be scientifically sound and acceptable for assessing risk to 

marine/estuarine invertebrates. The studies demonstrated that mandipropamid was 

moderately toxic to mysid shrimp (96-h LC50: 1.7 ppm a.i.) and very highly toxic to eastern 
38

oyster shell deposition (96-h EC50: 0.91 ppm a.i.). The endpoints produced in these studies 

will be used to assess the risk of mandipropamid to marine/estuarine invertebrates 

specifically mollusk and arthropod species (Table 12). 

(2). Chronic Effects 

Freshwater Fish

Mandipropamid is mobile and is likely to readily and frequently (due to multiple applications 

during a growing season) reach surface water bodies. Thus, a fish early life stage toxicity 

study testing mandipropamid is required (40CFR Part 158) to evaluate the potential for 

reproductive effects. The registrant submitted an early life-stage study testing the technical 

grade mandipropamid on fathead minnow (MRID 468001-08). The study was classified as 

scientifically sound and acceptable for use in assessing risk. The most sensitive endpoint in 

this study was on fish growth. The NOAEC for this endpoint was 0.22 ppm a.i.. This 

endpoint will be used to assess the chronic risk of mandipropamid use to freshwater fish. 

Freshwater Invertebrates

Mandipropamid is mobile and is likely to readily and frequently (due to multiple applications 

during a growing season) reach surface water bodies. Thus, invertebrate chronic toxicity 

testing mandipropamid is required (40CFR Part 158) to evaluate chronic effects to use of 

mandipropamid. The freshwater invertebrate reproductive toxicity study submitted by the 

registrant (MRID 468001-07) was deemed scientifically unsound for use in a risk assessment 

because of significant deviations from the guidelines for an invertebrate reproductive toxicity 

test. The reviewer’s analysis showed that reproduction of solvent control daphnids was 

significantly lower than that of negative control daphnids, which according to the EPA memo 

titled, “Interim Policy Guidance for the Use of Dilution-Water (Negative) and Solvent 

Controls in Statistical Data Analysis for Guideline Aquatic Toxicology Studies”, dated 

March 30, 2006, would result in the invalid classification of this study. 

Estuarine/Marine Fish

Currently, no estuarine and marine fish chronic toxicity studies have been submitted to the 

Agency. 

Estuarine/Marine Invertebrates

Currently, no estuarine and marine invertebrate chronic toxicity studies have been submitted 

to the Agency. 
39

(3). Sublethal Effects 

Freshwater Fish

All of the acute freshwater fish toxicity studies were reviewed and identified as scientifically 

unsound (MRID’s 468001-05, 468001-06, and 468001-04). Thus, although sublethal effects 

(loss of equilibrium, lethargy, surfacing, lying on the bottom of the aquarium) were observed 

in these studies, the dissolved concentrations at which these occur can not be determined. 

The most significant sublethal effects demonstrated by the freshwater fish chronic toxicity 

study were adverse effects on fish growth at a NOAEC of 0.210 ppm (MRID 468001-08). 

Sublethal effects noted in acute studies (loss of equilibrium, lethargy, surfacing, lying on the 

bottom of the aquarium) were not observed in juveniles in the fish early life stage test. 

Freshwater Invertebrates

The only sublethal effects reported for the freshwater invertebrate toxicity studies were in the 

study testing the mandipropamid degradate, CGA380778. The study reported the test 

organism (daphnia magna) having slow and/or lethargic movement during the test 

termination at 4.6 – 65 ppm (MRID’s 468001-51). 

Estuarine/Marine Fish

All of the acute marine/estuarine fish toxicity studies were reviewed and identified as 

scientifically unsound (MRID 468001-03 and –05). Thus, although sublethal effects (erratic 

swimming, loss of equilibrium, lying on the bottom of test vessel, lethargy) were observed in 

these studies, the dissolved concentrations at which these occur cannot be determined. 

Estuarine/Marine Invertebrates

Except for the effect on shell deposition no other sublethal effects were reported in the shell 

deposition or mysid shrimp studies (MRID’s 468001-02, and 468001-01). 

(4). Field Studies 

No aquatic field studies for mandipropamid were submitted. 

Plants Inhabiting Aquatic Areas

The registrant has submitted a nonvascular aquatic plant toxicity study testing the effect of 

mandipropamid on the green alga, Pseudokirchneriella subcapitata (MRID 468001-21) and a 

vascular aquatic plant toxicity study testing the effect of mandipropamid on Lemna gibba

(MRID 468001-19). Both studies of these studies are acceptable for aquatic plant toxicity 

requirements. The green algal study demonstrated an EC50 > 2.5 ppm a.i. for all endpoints 
40

measured and a NOAEC of 1.3 ppm based on biomass. The Lemna gibba study 

demonstrated an EC50 > 7.9 ppm a.i. for all endpoints measured and a NOAEC of 1.3 based 

on growth rate. These endpoints will be used to assess the risk of mandipropamid to aquatic 

nonvascular and vascular plants respectively. 

The registrant has also submitted a nonvascular aquatic plant toxicity study testing the effect 

of CGA380778, a mandipropamid degradate, on Pseudokirchneriella subcapitata (MRID 

468001-20). This study was reviewed and identified as a scientifically sound and an 

acceptable study for estimating risks to aquatic plants. The EC50 and NOAEC values 

produced in the study were 16 ppm and 2.4 ppm respectively. Since the aquatic plant 

toxicity studies testing the parent, mandipropamid, demonstrated a more sensitive NOAEC 

values than the study testing CGA380778 (a NOAEC of 1.3 ppm for the parent vs. a NOAEC 

of 2.4 for CGA380778), the risk to aquatic plants will be assessed solely based on the parent 

toxicity data.

2. Terrestrial Effects Characterization 

The most sensitive acute and chronic toxicity values associated with mandipropamid 

exposure to mammals, birds, and terrestrial plants are summarized in Table 14. These values 

are used to assess risk to terrestrial animals. All toxicity endpoint values utilized to assess the 

potential terrestrial risks of mandipropamid exposure were obtained from studies testing the 

technical grade mandipropamid. Except for an earthworm acute toxicity study testing, 

CGA380778, no other terrestrial organism toxicity tests were available testing any of the 

mandipropamid formulated products or mandipropamid degradates or metabolites. A more 

detailed summary of all available terrestrial toxicity data used to characterize effects 

associated with mandipropamid is given in Appendix E. 
41

Table 14. Mandipropamid Selected Toxicity Values for Screening Risk to Terrestrial 

Organisms 

Selected Test and Measurement Endpoints Assessment 

Endpoint 

Measures of 

Effect Species Toxicity 

Value 

Study 

Conditions 

Basis for 

Selection 

Reference 

(Classification)

1a. Avian 

(single dose) 

acute oral LD50

Mallard duck LD50 >1000 

mg a.i./kgbw(a)

(no mortality 

observed) 

TGAI, 96.5% 

a.i., Single dose, 

18weeks of age 

Lowest 

value of 

the two 

species 

tested 

MRID 468001-10

(Acceptable) 

1b. Avian 

subacute 5-day 

dietary LC50

Mallard duck 

and Bobwhite 

quail 

5-d LC50 > 

6080 mg 

a.i./kg diet(a)

(no mortality 

observed) 

TGAI, 96.5% 

a.i., 8-d test, 5-d 

exposure in 

food, 10 days 

old 

Both 

available 

studies 

were of 

equal 

sensitivity 

MRID 468001-12

(Acceptable) 

MRID 468001-13

(Acceptable) 

Abundance 

(i.e., survival, 

reproduction, 

and growth) of 

individuals 

and 

populations of 

birds in close 

proximity to 

sites 

1c. Avian 

reproduction 

NOAEL 

Mallard duck 

and Bobwhite 

quail 

NOAEC >

1060 mg 

a.i./kg diet(c)

TGAI, 20-week 

avian 

reproduction 

study, exposed 

via food 

Both 

available 

studies 

were of 

equal 

sensitivity 

MRID 

468001-14 

(Acceptable) 

MRID 

468001-15 

(Acceptable) 

2a. Mammalian 

acute oral 

(single dose) 

LD50

Abundance No data -- -- -- -- 

(i.e., survival, 

reproduction, 

and growth) of 

individuals 

and 

populations of 

mammals in 

close 

proximity to 

sites 

2b. Mammalian 

reproductive 

NOAEC or 

NOAEL 

Laboratory 

Rat 

(Rattus 

norvegicus) 

NOAEC = 250 

ppm a.i.(a)

(based on most 

sensitive 

endpoints: 

decreased 

body weights, 

weight gains, 

food 

consumption, 

and food 

utilization) 

TGAI, Twogeneration, 

exposure via 

food 

Most 

sensitive 

study 

(only 

study 

available) 

MRID 46800230

(Acceptable) 

Survival of 

beneficial 

insect 

populations in 

close 

proximity to 

sites 

Honey bee 

acute contact 

LD50

Honey bee 

(Apis 

mellifera L.) 

72-h LC50

>200 ug 

a.i./bee 

TGAI, applied to Most 

sensitive 

(only 

study 

available) 

468001-16 

(Acceptable) 
42

Table 14. Mandipropamid Selected Toxicity Values for Screening Risk to Terrestrial 

Organisms 

Selected Test and Measurement Endpoints Assessment 

Endpoint 

Measures of 

Effect Species Toxicity 

Value 

Study 

Conditions 

Basis for 

Selection 

Reference 

(Classification)

6a. Monocot 

seedling 

emergence 

EC25

All monocot 

species tested 

including 

corn, oat, 

onion, 

ryegrass 

>0.660 lbs 

a.i./A 

Mandipropamid 

Formulation 

A12496B 

All four 

monocots 

tested 

were 

equally 

sensitive 

468001-17 

(Acceptable) 

Dicot seedling 

emergence 

EC25

All dicot 

species tested 

except for 

carrot which 

produced 

unreliable 

results. The 

other tested 

dicot species 

included 

cucumber, 

radish, 

soybean, 

sugar beet, 

and tomato 

>0.660 lbs 

a.i./A 

Manipropamid 

formulation 

A12496B 

Most 

sensitive 

of the 

validated 

endpoint 

of the 

dicots 

tested 

468001-17 

(Supplemental) 

6b. Monocot 

seedling 

emergence 

NOAEC 

corn, oat, 

onion, and 

ryegrass 

0.660 lbs 

a.i./A 

Mandipropamid 

formulation 

A12496B 

All four 

monocots 

tested 

were 

equally 

sensitive 

468001-17 

(Acceptable) 

Dicot seedling 

emergence 

NOAEC 

cucumber, 

and soybean 

0.165 lbs 

a.i./A 

Mandipropamid 

formulation 

A12496B 

Most 

sensitive 

validated 

endpoint 

of the 

dicots 

tested. 

468001-17 

(Supplemental) 

6c. Monocot 

vegetative 

vigor EC25

corn, oat, 

onion, 

ryegrass 

>0.792 lbs 

a.i./A 

Mandipropamid 

formulation 

A12496B 

All four 

monocots 

tested 

were 

equally 

sensitive 

468001-18 

(Acceptable) 

Survival and 

growth of 

terrestrial 

plants in close 

proximity to 

sites 

Dicot 

vegetative 

vigor EC25

carrot, 

cucumber, 

radish, 

soybean, 

sugar beet, 

tomato 

>0.792 lbs 

a.i./A 

Mandipropamid 

formulation 

A12496B 

All six 

dicots 

tested 

were 

equally 

sensitive 

468001-18 

(Acceptable) 
43

Table 14. Mandipropamid Selected Toxicity Values for Screening Risk to Terrestrial 

Organisms 

Selected Test and Measurement Endpoints Assessment 

Endpoint 

Measures of 

Effect Species Toxicity 

Value 

Study 

Conditions 

Basis for 

Selection 

Reference 

(Classification)

6d. Monocot 

vegetative 

vigor NOAEC 

oat 0.198 lb a.i./A Mandipropamid 

formulation 

A12946B 

Most 

sensitive 

of the 

four 

monocots 

tested 

468001-18 

(Acceptable) 

Dicot 

vegetative 

vigor NOAEC 

Carrot, 

cucumber, 

radish, 

soybean, 

sugar beet, 

tomato 

0.792 lb a.i./A Mandipropamid 

formulation 

A12946B 

All six 

species 

tested 

were 

equally 

sensitive 

468001-18 

(Acceptable) 

(a) Note: Since, acute toxicity studies in birds demonstrated acute toxicity (LC50 or LD50) values higher than the 

highest concentrations tested and resulted in no mortalities, acute risk quotients will not be derived for birds. 

a. Terrestrial Animals 

(1). Acute Effects 

Birds

An acute oral toxicity study and two subacute dietary studies using the technical grade of the 

active ingredient (TGAI) are required (40CFR Part 158) to establish the acute toxicity of 

mandipropamid to birds. The preferred test species are a waterfowl (Mallard duck) and an 

upland gamebird (Northern bobwhite quail). Two studies were submitted by the registrant 

evaluating the acute oral toxicity and acute dietary toxicity of the technical grade of 

mandipropamid on Bobwhite quail and the Mallard duck (MRID’s 468001-10, 468001-11, 

468001-12, and 468001-13, respectively). All four studies were reviewed and identified to 

be scientifically sound and classified as acceptable for use in assessing risks to birds. No 

mortalities were observed in acute oral exposures to mandipropamid at up to 1000 mg a.i./kgbw (highest concentration tested) for the Mallard duck and at up to 2250 mg a.i./kg-bw for 

the Northern bobwhite quail or in acute dietary exposure to mandipropamid at up to 6080 

ppm a.i. for both species. Thus, mandipropamid is classified as practically nontoxic to avian 

species on an acute basis. 
44

Mammals

Wild mammal testing is required on a case-by-case basis, depending on the results of lower 

tier laboratory mammalian studies, intended use pattern and pertinent environmental fate 

characteristics. In most cases, rat or mouse toxicity values obtained from the Agency's 

Health Effects Division (HED) substitute for wild mammal testing. The registrant has 

submitted one acute oral mammalian toxicity study testing mandipropamid toxicity on rats 

(MRID 46800202). The study demonstrated mandipropamid is practically nontoxic to 

mammals (LD50 > 5000 mg/kg). 

Terrestrial Invertebrates

A honey bee acute contact study using the TGAI is required for mandipropamid because its 

proposed uses may result in honey bee exposure. An acceptable 72-hour contact toxicity 

study of technical grade mandipropamid in honey bees yielded a LD50 >200 μg a.i./bee 

(MRID 468001-16), indicating that technical grade mandipropamid is practically non-toxic 

to honey bees. This value was used to screen for risks to terrestrial beneficial insects. 

A scientifically sound earthworm acute toxicity study testing the technical grade 

mandipropamid (MRID 468001-22) and an earthworm acute toxicity study testing the 

mandipropamid degradate, CGA380778, (MRID 468001-23) were submitted to the Agency. 

No earthworm mortality was observed in either study the highest concentration tested was 

1000 mg a.i./kg of soil. 

(2). Chronic Effects 

Birds

There were two registrant submitted avian reproductive toxicity studies testing technical 

grade mandipropamid. The test organisms in these studies were Bobwhite quail and Mallard 

duck. Both studies demonstrated that mandipropamid did not cause any significant effects on 

reproduction or growth and survival of chicks at 1060 ppm a.i. which was the highest 

concentration tested. This value was used to screen for chronic reproductive risks. 

Mammals

There is one registrant submitted rat multigenerational reproductive toxicity study (MRID 

468002-30). The results of the study demonstrated a parental systemic NOAEL and 

offspring NOAEL of 250 ppm a.i. based on decreased parental body weights, decreased 

parental weight gains, decreased parental food consumption, decreased parental food 

utilization, decreased pup body weights in both sexes and delayed sexual maturation in 

offspring. The NOAEL of 250 ppm a.i. produced in this study will be used to assess the 

chronic risk of mandipropamid to mammals. 
45

Terrestrial Invertebrates

No chronic toxicity study was submitted for technical grade mandipropamid, its 

formulations, or degradates for terrestrial invertebrates. 

(3). Sublethal Effects 

Birds

In the acute oral toxicity study testing the acute oral effect of technical grade mandipropamid 

on bobwhite quail study, the only sublethal effects were the appearance of ruffled feathers on 

one bird in the control group and in five birds from the 2250 mg a.i./kg bw group. All birds 

appeared normal in appearance after 4 hours of dosing. Although the ruffled appearance may 

have been due to stress caused by handling during dosing, a treatment-related effect could 

not be precluded (MRID 468001-10). No similar sublethal effects were observed in the 

dietary study with bobwhite quail (MRID 468001-13) or in the acute oral toxicity and dietary 

studies with Mallard ducks (MRID 468001-11 and –12, respectively). 

In the acute oral toxicity study testing mandipropamid on the Mallard duck the only sublethal 

effects were four females in the 1000 mg a.i./kg-bw group observed drinking frequently 

during the first 2 hours following dosing. No birds, however, from this level were observed 

to regurgitate. In the 1500 mg a.i./kg-bw group, one female and two males were observed 

drinking frequently, almost immediately following dosing. Both females that were observed 

drinking frequently were observed regurgitating approximately 30 minutes following dosing. 

One male was also observed regurgitating approximately 1 hour and 20 minutes following 

dosing. All birds were normal in appearance and behavior by 3.5 hours following dosing. 

Based on regurgitation, the NOAEL for clinical signs of toxicity was 1000 mg a.i./kg-bw 

(MRID 468001-11). 

Both acute dietary studies demonstrated visually determined treatment related decrease in 

body at the highest concentration tested which was 6080 ppm a.i. (MRID’s 468001-12 and 

468001-13).

Mammals

Based on the available mammalian toxicity data, the only sublethal effects of mandipropamid 

to mammals was demonstrated in the rat multigenerational study (MRID 46800230). The 

sublethal effects demonstrated in this study were decreased parental body weights, decreased 

parental weight gains, decreased parental food consumption, decreased parental food 

utilization, decreased pup body weights in both sexes and delayed sexual maturation in 

offspring. The NOAEL of these effects were 250 ppm a.i.. 
46

Terrestrial Invertebrates

The only terrestrial invertebrate studies which demonstrated any sublethal effects were the 

mandipropamid and CGA380778 earthworm toxicity studies (MRID’s 468001-22 and 

468001-23). The sublethal effects in the studies included significant reductions in percent 

weight loss which were demonstrated at a NOAEC of 320 mg/kg of soil and a LOAEC of 

1000 mg/kg of soil for the study testing mandipropamid and at a NOAEC of 100 mg/kg of 

soil and a LOAEC 1000 mg/kg of soil for the study testing CGA380778. 

(4). Field Studies 

No field studies were submitted for mandipropamid or any of its degradates. 

b. Terrestrial Plants 

The registrant submitted a seedling emergence and vegetative vigor study testing the A12946B, 

the formulation containing the active ingredient Mandipropamid. The following summarizes the 

results of both studies. 

The effect of A12946B on the seedling emergence of monocot (corn, Zea mays; oat, Avena 

sativa; onion, Allium cepa; and ryegrass, Lolium perenne) and dicot (carrot, Daucus carota; 

cucumber, Cucumis sativa; radish, Raphanus sativus; soybean, Glycine max; sugar beet, Beta 

vulgaris; and tomato, Lycopersicon esculentum) crops was studied at nominal application rates 

of 0 (negative and surfactant controls), 0.0413, 0.0825, 0.165, 0.330 and 0.660 lbs a.i./A. The 

growth medium used in the seedling emergence test was natural soil, classified as a loam soil, 

with an organic matter content of 1.7% (1.0% organic carbon) and an adjusted pH of 7.4. On 

day 21 the surviving plants per pot were recorded and cut at soil level for measuring the plant 

height and dry weight. 

Dry weight was significantly affected in cucumber, soybean and tomato, but reductions did not 

exceed 25%. The percent inhibition in seedling emergence in the treated species as compared to 

the control ranged from -4 to 8%. No monocot species were sensitive to treatment, but an EC05

value could be calculated for corn dry weight. Carrot was the only dicot species to exhibit a 

reduction of ≥25% (based on dry weight) relative to the negative control; however, the response 

was not dose-dependent, with the three lowest treatment groups experiencing increases in dry 

weight of 2-21%. The reviewer was unable to determine reliable ECx values for carrot dry 

weight. Additionally, one replicate in the highest treatment group failed to emerge and overall 

emergence of the controls and treatment groups was fairly low (60-73%). This implies that 

factors other than treatment contributed to the poor performance of carrot in this study. The 

study was deemed supplemental because of this study deficiency. 

The effect of A12946B on the vegetative vigor of monocot (corn, Zea mays; oat, Avena sativa; 

onion, Allium cepa; and ryegrass, Lolium perenne) and dicot (carrot, Daucus carota; cucumber, 

Cucumis sativa; radish, Raphanus sativus; soybean, Glycine max; sugar beet, Beta vulgaris; and 

tomato, Lycopersicon esculentum) crops was studied at nominal application rates of 0 (negative 
47

and surfactant controls), 0.0495, 0.0994, 0.198, 0.396 and 0.792 lbs a.i./A. The growth medium 

used in the test was an artificial soil that represented a loam soil and was composed of a mixture 

of kaolinite clay, industrial quartz sand and peat; the organic matter content was 1.7% (1.0% 

organic carbon) and the pH was 7.4. On day 21 the surviving plants per pot were recorded and 

cut at soil level for measuring the plant height and dry weight. 

In the vegetative vigor test, plant height was affected by A12946B treatment in oat only. Dry 

weight, plant height and survival were not affected in any other species. The most sensitive 

monocot species, based on plant height, in the vegetative vigor test was oat with an EC25 of 

>0.792 lbs a.i./A and a NOAEC of 0.198 lbs a.i./A. No dicot was sensitive to treatment, so the 

EC25 value was >0.792 lbs a.i./A and the NOAEC values was 0.792 lbs a.i./A (the highest 

concentration tested). 

The study was deemed acceptable for a Tier II vegetative vigor terrestrial plant toxicity study. 
48

IV. RISK CHARACTERIZATION 

Risk characterization is the integration of exposure and effects characterization to determine 

the ecological risk from the use of mandipropamid and the likelihood of effects on aquatic 

life and wildlife based on all the proposed uses at the maximum proposed use rate. The risk 

characterization provides estimation and description of the risk; articulates risk assessment 

assumptions, limitations, and uncertainties; synthesizes an overall conclusion; and provides 

the risk managers with information to make regulatory decisions. 

A. Risk Estimation – Integration of Exposure and Effects Data 

Results of the exposure and toxicity effects data are used to evaluate the likelihood of 

adverse ecological effects on non-target species. For the assessment of mandipropamid risks, 

the risk quotient (RQ) method is used to compare exposure and measured toxicity values. 

Estimated environmental concentrations (EECs) for acute and chronic exposure are divided 

by acute and chronic toxicity values, respectively. The resulting RQs are then compared to 

the Agency’s levels of concern (LOCs). The LOCs, as summarized in the Risk 

Characterization Section, are the Agency’s interpretive policy used to analyze potential risk 

to non-target organisms and the need to consider regulatory action. 

1. Non-Target Aquatic Animals and Plants 

To assess risks of mandipropamid on all proposed uses to non-target aquatic organisms (i.e., 

fish, invertebrates, plants), surface water EECs for total residues of mandipropamid including 

its degradates of toxic concern, SYN500003 and SYN504851 (as identified by HED), were 

obtained using GENEEC based on the maximum proposed label rate of 4 applications, 7 

days apart at 0.13 lbs a.i./A. The instaneous peak concentration is used to derive RQs for 

acute exposure and the 21-day and 60-day peak exposure concentrations were used to derive 

RQ values for chronic exposure to invertebrates and fish, respectively. The most sensitive 

toxicity values for the TGAI mandipropamid were used to calculate risk quotients for aquatic 

organisms exposed to mandipropamid. 

a. Acute Risk to Animals (Fish and Invertebrates) 

Only acute RQ values for freshwater and marine/estuarine invertebrates were calculated. 

According to the acute RQ values for aquatic invertebrates, mandipropamid does not pose a 

risk to freshwater or marine/estuarine invertebrates above the Agency’s Level of Concern 

(see Table 15). Acute RQ values could not be calculated for freshwater and marine/estuarine 

fish because all the acute fish toxicity data were deemed invalid. 
49

Table 15. Acute RQs for Aquatic Organisms Exposed to Mandipropamid 

including its degradate of toxic concern, SYN500003 and SYN504851. 

Measure of Effect(Test 

Species) 

Toxicity 

Value 

(ppm) 

EEC 

Peak 

(ppm) 

Acute RQ 

(EEC/Toxicity Value) 

Freshwater Invertebrates (Test 

Species: Water flea) 

48-h EC50 7.l 0.021 0.003 * 

Marine/Estuarine Invertebrates 

(Test Species: Mysid Shrimp) 

96-h LC50 1.7 0.021 0.01 * 

Marine/Estuarine Invertebrates 

(Test Species: Eastern Oyster) 

96-h EC50 0.91 0.021 0.02 * 

* Does not exceed acute endangered species LOC of 0.05 or acute LOC of 0.1 

b. Chronic Risk to Aquatic Animals (Fish and Invertebrates) 

Only a chronic RQ for freshwater fish from exposure to mandipropamid was calculated. 

Chronic RQ values for estuarine and marine fish and invertebrates and freshwater 

invertebrates from exposure to mandipropamid could not be calculated because either the 

submitted data were invalid or no study was submitted. Based on the freshwater fish chronic 

RQ value, mandipropamid does not pose a chronic risk to fish (Table 16). 

Table 16. Chronic RQs for Aquatic Organisms Exposed to Mandipropamid

Chemical 

Measure of Effect (Test 

Species) 

NOAEC 

(ppm) 

60 day EEC 

value (ppm) 

Chronic RQ 

(EEC/NOAEC)

Mandipropamid Freshwater fish (Test Species: 

Fathead minnow) 

0.210 0.0095 0.05 * 

* Does not exceed chronic LOC of 1. 
50

c. Risks to Aquatic Plants 

Based on the RQ calculations for aquatic plants, mandipropamid usage is not expected to 

exceed the Agency’s Level of Concern for risk to aquatic plants (Table 17). 

Table 17. Risk Quotients for Aquatic Plants Algae Exposed to the Mandipropamid

Type of aquatic 

plant Organism 

4-d 

EC50

(ppm) 

4-d 

NOAEC 

(ppm) 

EEC 

Peak 

(ppm) 

RQ 

Non-Listed 

(EEC/EC50) 

RQ 

Listed 

(EEC/NOAEC) 

Aquatic vascular 

plant 

Duck weed 

(Lemna gibba) 

> 7.9 1.3 0.021 < 1 0.02* 

Aquatic 

nonvascular plant 

>2.5 

ppm 

1.3 0.021 < 1 0.02* 

* Does not exceeds endangered or non-endangered species LOC (1) 

2. Non-Target Terrestrial Animals 

To assess risks of mandipropamid to non-target terrestrial animals, EECs and acute and 

chronic RQs for residues on various forage categories (short grass, tall grass, broadleaf 

plants/small insects, fruits/pods/large insects, and seeds) were obtained from the Tier I model 

T-REX for maximum proposed application rates. An explanation of the model is presented 

in Appendix C. 

a. Acute Risk to Mammals and Birds 

Acute RQ values for avian or mammalian species were not calculated because the highest 

concentration or dosages tested in the acute dietary test (6080 ppm) and acute oral test 

(>1000 mg/kg-bw) for both a Mallard duck and Northern bobwhite and the acute oral test for 

mammals (> 5000 mg/kg) did not result in any mortality (MRID 468001-10, 468001-11, 

468001-12, and 468001-13). Therefore at the highest dietary residue level (103 ppm) no 

mortality from mandipropamid is likely given that no mortality was observed at 

concentrations 60 times above this residue level in laboratory birds and mammals. 

b. Chronic Risk to Birds and Mammals 

Dietary-based chronic RQs for birds and mammals are summarized in Table 18. Chronic 

RQs for birds and mammals are below the chronic LOC (1) for all dietary residue categories. 
51

Table 18. Dietary-Based Chronic RQs for Birds and Mammals Based on Upper Bound Residues 

as Calculated by T-REX 

Avian Chronic Risk Quotients 

Based on Chronic NOAEC of 1060 ppm. 

Crop Use 

Short Grass Tall Grass 

Broadleaf 

Plants/Small 

Insects 

Fruits/Pods/ 

Large Insects 

All proposed crops (See Usage 

Overview Section 4.) 0.10* 0.04* 0.05* 0.01* 

* Note: Does not exceed the chronic LOC (1) for terrestrial animals. 

Mammalian Chronic Risk Quotients 

Based on a Chronic NOAEC of 250 ppm. 

Crop Use 

Short Grass Tall Grass 

Broadleaf 

Plants/Small 

Insects 

Fruits/Pods/ 

Large Insects 

All proposed crops (See Usage 

Overview Section 4.) 0.41* 0.19* 0.23* 0.03* 

* Note: Does not exceed the chronic LOC (1) for terrestrial animals 

c. Risk to Terrestrial Invertebrates 

Although EFED does not quantitatively assess risks to non-target terrestrial invertebrates, 

acute toxicity studies show that mandipropamid TGAI is practically non-toxic to honey bees 

and nontoxic to earthworms at the highest dose tested. Additionally, acute toxicity studies on 

the mandipropamid degradate, CGA380778, demonstrated that CGA380778 is nontoxic to 

earthworms at the highest dose tested. 

3. Non-target Plants Inhabiting Terrestrial and Semi-Aquatic Areas 

RQs were not calculated to determine mandipropamid’s risk to nontarget nonlisted terrestrial 

plant species because for all the plant species tested in the vegetative vigor study and 

seedling emergence study the validated EC25 values were above the highest levels tested. 

These test levels were above the highest proposed use rates. Thus, EFED does not expect 

mandipropamid to pose a significant risk to nonlisted terrestrial plants. Table 19 

demonstrates the listed terrestrial plant RQs for mandipropamid based on the NOAEC values 

demonstrated in the terrestrial plant studies. The RQs indicate that mandipropamid does not 

pose a risk to listed terrestrial plants that exceeds the Agency’s Level of Concern. 
52

Table 19. Risk Quotients for Non-Listed Species and Listed Species Terrestrial and Semi-Aquatic 

Plant Emergence in Areas Adjacent to Treatment Sites (due to drift) for Mandipropamid 

Risk Quotients b

Terrestrial Plant 

Emergence 

(Adjacent Area) 

Semi-Aquatic Plant 

Emergence 

(Adjacent Area) 

Terrestrial Plant 

Vegetative Vigor 

(Drift) 

Application 

Rate (lbs 

a.i./acre) Crop Use Monocot Dicot Monocot Dicot Monocot Dicot 

Listed Terrestrial and Semi-Aquatic Plant

0.14 All 

proposed 

uses at the 

maximum 

application 

rate 

0.006 c 0.02 c 0.04 c 0.17 c 0.0001 c 0.0001 c

a

 RQs are calculated using TerrPlant. See Appendix D for explanation TerrPlant model. b

 Based on the NOAEC values = 0.165 lb a.i./acre and 0.660 lb a.i./acre for seedling emergence study in dicots and monocots 

respectively and NOAEC = 0.792 for vegetative vigor in monocots and dicots. c

 Does not Exceed Listed Species LOC for Terrestrial and Semi-Aquatic Plants (≥1) 

B. Risk Description 

1. Risks to Aquatic Organisms 

Based on risk estimates, the proposed mandipropamid uses are not expected to pose a 

significant 

• acute risk to freshwater or marine and estuarine invertebrates 

• acute risk to aquatic plants 

• chronic risk to freshwater fish. 

These conclusions are based on the premise that the RQ values for acute risk to aquatic 

invertebrate, acute risk to plants, and chronic risk to fish are several orders of magnitude 

below the Agency LOC. Currently, EFED is unable to definitively determine whether 

mandipropamid poses an acute risk to fish because of the lack of acceptable fish acute 

toxicity data. 

2. Risks to Terrestrial Organisms 

a. Terrestrial Animals (Mammals and Birds) 

Based on available registrant submitted data, mandipropamid is not expected to pose a 

significant chronic or acute risk to birds or mammals. 

EFED avian and mammal acute and chronic risk conclusions are based on the fact that the 

acute toxicity studies in birds and mammals failed to establish acute lethality values, with no 

mortalities at the highest doses/concentrations tested and the RQs for chronic risk to birds 
53

were several orders of magnitude lower than the Agency Level of Concern for avian chronic 

risk. 

EFED’s conclusion regarding the chronic mammalian risk is based on the premise that the 

chronic RQ values (derived from the rat multigenerational NOAEC of 250 ppm based on 

decreases in body weight, weight gains, food consumption, and food utilization) were more 

than 2 times less than the LOC for chronic dietary risk. Thus, EFED does not expect 

mammalian chronic exposure to mandipropamid to be a significant risk. 

b. Insects 

Although EFED does not derive RQ values for non-target insects, risks can be assessed 

qualitatively. Results of toxicity studies on technical grade mandipropamid show that the 

compound is practically non-toxic to honey bees on both a contact and an oral basis and non 

toxic to earthworms at the highest concentrations tested (1000 mg/kg in soil). Therefore, 

acute risks of technical grade mandipropamid exposure to pollinators and other beneficial 

insects are not anticipated. 

c. Plants 

Formulated Product

EFED does not expect mandipropamid to pose a significant risk to terrestrial plants. This 

determination is based on the premise that the RQ values for plants are several orders of 

magnitude lower than the Agency LOC. 

There is some uncertainty regarding the plant emergence RQ values because they are based 

on a supplemental seedling emergence study. The study was deemed supplemental because 

the carrot species tested did not yield any reliable endpoint values. EFED assessed the plant 

emergence risk of mandipropamid based on the other 9 species tested (all of which 

demonstrated no significant risk from mandipropamid that exceeded the Agency LOC). 

Thus, there is some uncertainty whether plant species closely related to carrots may be 

adversely affected by mandipropamid, since EFED had no reliable test data on carrots. 

3. Review of Incident Data 

Incident reports submitted to EPA since approximately 1994 have been tracked by 

assignment of EIIS (Environmental Incident Information System) in an Incident Data System 

(IDS). Since mandipropamid is a new chemical and has not been previously approved for use 

in the U.S., there are no incident reports. 

4. Endocrine Effects 

None of the available data indicate that mandipropamid may have detrimental effects on the 

endocrine system. 
54

C. Federally Threatened and Endangered (Listed) Species Concerns 

1. Action Area 

For listed species assessment purposes, the action area is considered to be the area affected 

directly or indirectly by the Federal action and not merely the immediate area involved in the 

action. At the initial screening level, the risk assessment considers broadly described 

taxonomic groups and so conservatively assumes that listed species within those broad 

groups are collocated with the pesticide treatment area. This means that terrestrial plants and 

wildlife are assumed to be located on or adjacent to the treated site and aquatic organisms are 

assumed to be located in a surface water body adjacent to the treated site. The assessment 

also assumes that the listed species are located within an assumed area which has the 

relatively highest potential exposure to the pesticide, and that exposures are likely to decrease 

with distance from the treatment area. This risk assessment presents the use of 

mandipropamid on all proposed uses including brassica, leafy greens, bulb vegetables, 

cucurbits, grapes, leafy vegetables, peppers, and other fruiting vegetables and establishes 

initial collocation of species with treatment areas. 

If the assumptions associated with the screening level assessment result in RQs that are 

below the listed species LOCs, a "no effect" determination conclusion is made with respect 

to listed species in that taxa, and no further refinement of the action area is necessary. 

Furthermore, RQs below the listed species LOCs for a given taxonomic group indicate no 

concern for indirect effects upon listed species that depend upon the taxonomic group 

covered by the RQ as a resource. However, in situations where the screening assumptions 

lead to RQs in excess of the listed species LOCs for a given taxonomic group, a potential for 

a "may affect" conclusion exists and may be associated with direct effects on listed species 

belonging to that taxonomic group or may extend to indirect effects upon listed species that 

depend upon that taxonomic group as a resource. In such cases, additional information on the 

biology of listed species, the locations of these species, and the locations of use sites could be 

considered to determine the extent to which screening assumptions regarding an action area 

apply to a particular listed organism. These subsequent refinement steps could consider how 

this information would impact the action area for a particular listed organism and may 

potentially include areas of exposure that are downwind and downstream of the pesticide use 

site. 

2. Taxonomic Groups Potentially at Risk 

This screening level risk assessment indicates that uses of mandipropamid will have: 1) no 

direct or indirect acute risk to listed aquatic invertebrates, 2) no direct or indirect chronic risk 

to fish, 3) no direct or indirect acute or chronic risk to birds, 3) no direct or indirect acute or 

chronic risk to mammals, and no direct risk to aquatic plants. Currently, EFED cannot 

definitively determine the acute risk to fish, or chronic risk to aquatic invertebrate because of 

the lack of acceptable toxicity data for these organisms. 
55

The Agency has developed the Endangered Species Protection Program to identify pesticides 

whose use may cause adverse impacts on endangered and threatened species, and to 

implement mitigation measures that address these impacts. The Endangered Species Act 

(ESA) requires federal agencies to ensure that their actions are not likely to jeopardize listed 

species or adversely modify designated critical habitat. To analyze the potential of registered 

pesticide uses that may affect any particular species, EPA uses basic toxicity and exposure 

data and considers it in relation to individual species and their locations by evaluating 

important ecological parameters, pesticide use information, geographic relationship between 

specific pesticide uses and species locations, and biological requirements and behavioral 

aspects of the particular species, as part of a refined use and species-specific analysis. When 

conducted, this species-specific analysis will take into consideration any regulatory changes 

that have been implemented at that time. 

3. Probit Dose Response Relationship 

Because there were no LOC exceedances for any organisms based on any of the available 

data a Probit Analysis was not warranted. 

4. Indirect Effects Analysis 

Because there were no LOC exceedances for any organisms based on any of the available 

data an indirect effects analysis was not warranted. 

5. Critical Habitat 

In the evaluation of pesticide effects on designated critical habitat, consideration is given to 

the physical and biological features (constituent elements) of a critical habitat identified by 

the U.S Fish and Wildlife and National Marine Fisheries Services as essential to the 

conservation of a listed species and which may require special management considerations or 

protection. The evaluation of impacts for a screening level pesticide risk assessment focuses 

on the biological features that are constituent elements and is accomplished using the 

screening level taxonomic analysis (RQs) and listed species’ levels of concern (LOCs) that 

are used to evaluate direct and indirect effects to listed organisms. 

Because there were no LOC exceedances for any organisms based on any of the available 

data an identification of any endangered species critical habitat was not warranted. 
56

D. Description of Assumptions, Limitations, Uncertainties, Strengths and Data 

Gaps 

1. Assumptions, Limitations, Uncertainties, Strengths and Data Gaps 

Related to Exposure for All Taxa 

There are a number of areas of uncertainty in the aquatic and terrestrial risk assessments. The 

toxicity assessment for terrestrial and aquatic animals is limited by the number of species 

tested in the available toxicity studies. Use of toxicity data on representative species does not 

provide information on the potential variability in susceptibility to acute and chronic 

exposures. 

This screening level risk assessment relies on labeled statements of the maximum rate of 

mandipropamid application, the maximum number of applications, and the shortest interval 

between applications. Together, these assumptions constitute a maximum use scenario. The 

frequency at which actual uses approach these maximums is dependant on resistance to the 

fungicide, timing of applications, and market forces. 

2. Assumptions, Limitations, Uncertainties, Strengths and Data Gaps 

Related to Exposure for Aquatic Species 

a. GENEEC 2.0 Model 

GENEEC is a single event model. It assumes one single large rainfall/runoff event occurs 

that removes a large quantity of pesticide from the field to the water all at one time. Longerterm, multiple-day average concentration values are calculated based on the peak day value 

and subsequent values considering degradation processes. This computer-based model 

utilizes basic chemical parameters (solubility, photolysis, hydrolysis, Koc, and soil 

degradation) combined with application rate and method of soil incorporation to determine 

the EEC. The model considers the reduction in dissolved pesticide residues due to adsorption 

to soil or sediment, incorporation depth, degradation in soil before washoff to a water body, 

and degradation of the residues within the water body. The model assumes that the runoff 

from a 10 hectare (24.7 acre) field is entering a 1 hectare (2.47 acre) by 2 meter (6.56 feet) 

deep pond. GENEEC is a more extensive mathematical model designed from output 

generated by the PRZM and EXAM models. However GENEEC is a generic, in that it does 

not consider differences in climate, soil, topography, or crop in estimating pesticide 

exposure. GENEEC is used as a tool to specifically estimate a pesticide concentration in a 

standard water body due to off-target movement of pesticide. This model has been used by 

OPP primarily in the first-tier risk assessment of pesticide exposure to aquatic life. 

OPP uses computer modeling (GENEEC) to estimate pesticide concentrations in an edge-ofthe-field pond for use in screening ecological exposure and risk assessments. Such modeling 

has also been used as a screen for drinking water assessments 

(http://www.epa.gov/oscpmont/sap/meetings/1997/december/finaldec.pdf). 
57

3. Assumptions, Limitations, Uncertainties, Strengths and Data Gaps 

Related to Exposure for Terrestrial Species 

a. Residue Concentration 

The data available to support the exposure assessment for mandipropamid is substantially 

complete, with the exception of a foliar dissipation study, which is an input variable for Tier I 

modeling of risks to birds and mammals (i.e., T-REX Model). The terrestrial modeling was 

conducted with a default foliar half-life of 35 days, which may not be realistic, however, is 

likely a conservative foliar half-life for this compound. 

b. Variation in Habitat and Dietary Requirements 

For screening terrestrial risk assessments, a generic bird or mammal is assumed to occupy 

either the treated field or adjacent areas receiving pesticide at a rate commensurate with the 

treatment rate on the field. The habitat and feeding requirements of the modeled species and 

the wildlife species may be different. It is assumed that species occupy, exclusively and 

permanently, the treated area being modeled. This assumption leads to a maximum level of 

exposure in the risk assessment. 

The acute studies have a fixed exposure period, not allowing for the differences in response 

of individuals to different durations of exposure. Further, for the acute oral study, 

mandipropamid is administered in a single dose which does not mimic wild birds’ exposure 

through multiple feedings. Also, it does not account for the effect of different environmental 

matrices on the absorption rate of the chemical into the animal. Because exposure occurs 

over several days, both the accumulated dose and elimination of the chemical from the body 

for the duration of the exposure determine the exact exposure to wildlife, however, they are 

not taken into account in the screening assessment. There was also no assumption of an effect 

of repeated doses that change the tolerance of an individual to successive doses. 

c. Variation in Diet Composition 

The risk assessment and calculated RQs assume 100% of the diet is relegated to single food 

types foraged only from treated fields. The assumption of 100% diet from a single food type 

may be realistic for acute exposures, but diets are likely to be more variable over longer 

periods of time. This assumption is likely to be conservative and will tend to overestimate 

potential risks for chronic exposure, especially for larger organisms that have larger home 

ranges. These large animals (e.g., deer and geese) will tend to forage from a variety of areas 

and move on and off of treated fields. Small animals (e.g., mice, voles, and small birds) may 

have home ranges smaller than the size of a treated field and will have little or no opportunity 

to obtain foodstuffs that have not been treated with mandipropamid. Even if their home range 

does cover area outside the treated field, mandipropamid may have drifted or runoff to areas 

adjacent to the treated field. 
58

d. Exposure Routes Other than Dietary 

Screening level risk assessments for spray applications of pesticides consider dietary 

exposure to terrestrial organisms. Other exposure routes are possible for animals residing in 

or moving through treated areas. These routes include ingestion of contaminated drinking 

water, ingestion of contaminated soils, preening/grooming, and dermal contact. Preening 

exposures, involving the oral ingestion of material from the feathers remains an unquantified, 

but potentially important, exposure route. If toxicity is expected through any of these other 

routes of exposure, then the risks of a toxic response to mandipropamid is underestimated in 

this risk assessment. Other routes of exposure, not considered in this assessment, are 

discussed below. 

e. Incidental Soil Ingestion Exposure 

This risk assessment does not consider incidental soil ingestion. Available data suggests that 

up to 15% of the diet can consist of incidentally ingested soil depending on the species and 

feeding strategy (Beyer et al. 1994). Although mandipropamid it is not expected to be 

persistent in soils, incidental ingestion of soil within days of mandipropamid application may 

be an important exposure pathway. 

f. Inhalation Exposure 

The screening risk assessment does not consider inhalation exposure, due to the low volatility 

of mandipropamid; it is not expected to be an important exposure pathway. 

g. Dermal Exposure 

The screening assessment does not consider dermal exposure. Dermal exposure may occur 

through three potential sources: (1) direct application of spray to terrestrial wildlife in the 

treated area or within the drift footprint; (2) incidental contact with contaminated vegetation; 

or (3) contact with contaminated water or soil. 

The available measured data related to wildlife dermal contact with pesticides are extremely 

limited. The Agency is actively pursuing modeling techniques to account for dermal 

exposure via direct application of spray and by incidental contact with vegetation. 

h. Drinking Water Exposure 

Drinking water exposure to a pesticide active ingredient may be the result of consumption of 

surface water or consumption of the pesticide in dew or other water on the surfaces of treated 

vegetation. Given that mandipropamid has a high solubility in water, there is the potential for 

mandipropamid to dissolve in runoff and puddles on the treated field. Consumption of 

drinking water would appear to be inconsequential if water concentrations were equivalent to 

the concentrations from PRZM/EXAMS; however, concentrations in puddled water sources 

on treated fields may be higher than concentrations estimated in the 1 ha pond used in 

EXAMS. Given that this exposure route is not included in the assessment, overall risk may 
59

be underestimated. Although the potential impact of discharging groundwater is not 

explicitly delineated, it should be noted that groundwater could provide a source of pesticide 

to surface water bodies – especially low-order streams, headwaters, and groundwater-fed 

pools. This is particularly likely if the chemical is persistent and mobile. Soluble chemicals 

that are only subject to photolytic degradation will be very likely to persist in groundwater, 

and can be transportable over long distances. Much of this groundwater will eventually be 

discharged to the surface – often supporting stream flow in the absence of rainfall. 

Continuously flowing low-order streams in particular are sustained by groundwater 

discharge, which constitutes 100% of stream flow during baseflow (no runoff) conditions. 

Thus, it is important to keep in mind that pesticides in groundwater can have a major 

(detrimental) impact on surface water quality. 

i. Dietary Intake – Differences Between Laboratory and Field 

Conditions 

Several aspects of the dietary test introduce uncertainty into calculation of the LC50 value 

(Mineau et al. 1994; ECOFRAM 1999). The endpoint of this test is reported as the 

concentration mixed with food that produces a response rather than as the dose ingested. 

Although food consumption sometimes allows for the estimate of a dose, calculations of the 

mg/kg/day dose are confounded by undocumented spillage of feed and how consumption is 

measured over the duration of the test. Usually, if measured at all, food consumption is 

estimated once at the end of the five-day exposure period. Furthemore, for studies in avian, 

group housing of birds undergoing testing only allows for a measure of the average 

consumption per day for a group; consumption estimates can be further confounded if birds 

die within a treatment group. The exponential growth of young birds also complicates the 

estimate of the dose; controls often nearly double in size over the duration of the test. Since 

weights are only taken at the initiation of the exposure period and at the end, the dose per 

body weight (mg/kg) is difficult to estimate with any precision. The interpretation of this test 

is also confounded because the response of birds is not only a function of the intrinsic 

toxicity of the pesticide, but also the willingness of the birds to consume treated food. 

Further, the acute and chronic characterization of risk rely on comparisons of wildlife dietary 

residues with LC50 or NOAEC values expressed in concentrations of pesticides in laboratory 

feed. These comparisons assume that ingestion of food items in the field occurs at rates 

commensurate with those in the laboratory. Although the screening assessment process 

adjusts dry-weight estimates of food intake to reflect the increased mass in fresh-weight 

wildlife food intake estimates, it does not allow for gross energy and assimilative efficiency 

differences between wildlife food items and laboratory feed. On gross energy content alone, 

direct comparison of a laboratory dietary concentration based effects threshold to a freshweight pesticide residue estimate would result in an underestimation of field exposure by 

food consumption by a factor of 1.25–2.5 for most food items. Only for seeds would the 

direct comparison of dietary threshold to residue estimate lead to an overestimate of 

exposure. 
60

Differences in assimilative efficiency between laboratory and wild diets suggest that current 

screening assessment methods do not account for a potentially important aspect of food 

requirements. Depending upon species and dietary matrix, bird assimilation of wild diet 

energy ranges from 23–80%, and mammal's assimilation ranges from 41–85% (USEPA 

1993). If it is assumed that laboratory chow is formulated to maximize assimilative efficiency 

(e.g., a value of 85%), a potential for underestimation of exposure may exist by assuming 

that consumption of food in the wild is comparable with consumption during laboratory 

testing. In the screening process, exposure may be underestimated because metabolic rates 

are not related to food consumption. 

Finally, the screening procedure does not account for situations where the feeding rate may 

be above or below requirements to meet free living metabolic requirements. Gorging 

behavior is a possibility under some specific wildlife scenarios (e.g., bird migration) where 

the food intake rate may be greatly increased. Kirkwood (1983) has suggested that an upperbound limit to this behavior might be the typical intake rate multiplied by a factor of 5. In 

contrast is the potential for avoidance, operationally defined as animals responding to the 

presence of noxious chemicals in their food by reducing consumption of treated dietary 

elements. This response is seen in nature where herbivores avoid plant secondary 

compounds. 

In the absence of additional information, the acute oral LD50 test provides the best estimate of 

acute effects for chemicals where exposure can be considered to occur over relative short 

feeding periods, such as the diurnal feeding peaks common to avian species (ECOFRAM 

1999). 

4. Assumptions, Limitations, Uncertainties, Strengths and Data Gaps 

Related to Effects Assessment 

a. Age Class and Sensitivity of Effects Thresholds 

It is generally recognized that test organism age may have a significant impact on the 

observed sensitivity to a toxicant. The screening risk assessment acute toxicity data for fish 

are collected on juvenile fish between 0.1 and 5 grams. Aquatic invertebrate acute testing is 

performed on recommended immature age classes (e.g., first instar for daphnids, second 

instar for amphipods, stoneflies, and mayflies, and third instar for midges). Similarly, acute 

dietary testing with birds is also performed on juveniles, with mallard ducks being 5–10 days 

old and bobwhite quail 10–14 days old. 

Testing of juveniles may overestimate toxicity of older age classes for pesticidal active 

ingredients, such as mandipropamid, that act directly (without metabolic transformation) 

because younger age classes may not have the enzymatic systems associated with detoxifying 

xenobiotics. The screening risk assessment has no current provisions for a generally applied 

method that accounts for this uncertainty. In so far as the available toxicity data may provide 

ranges of sensitivity information with respect to age class, the risk assessment uses the most 

sensitive life-stage information as the conservative screening endpoint. 
61

b. Use of the Most Sensitive Species Tested 

Although the screening risk assessment relies on a selected toxicity endpoint from the most 

sensitive species tested, it does not necessarily mean that the selected toxicity endpoint 

reflects sensitivity of the most sensitive species existing in a given environment. The relative 

position of the most sensitive species tested in the distribution of all possible species is a 

function of the overall variability in sensitivity among species to a particular chemical. In the 

case of listed species, there is uncertainty regarding the relationship of the listed species' 

sensitivity and the most sensitive species tested. 

The Agency is not limited to a base set of surrogate toxicity information in establishing risk 

assessment conclusions. When available, the Agency also considers toxicity data on nonstandard test species. 
62

V. REFERENCES 

Open Literature, Government Reports, and Product Labels

Beyer, W.N. 1994. Estimates of soil ingestion by wildlife. J Wildl Manage 58(2):375–382. 

Davis, G.E., P.L. Haaker, and D.V. Richards. 1996. Status and trends of white abalone at the 

California Channel Islands. Transactions of the American Fisheries Society 125:42–48. 

Fletcher, J.S., J.E. Nellesson, and T. G. Pfleeger. 1994. Literature review and evaluation of 

the EPA food-chain (Kenaga) nomogram, an instrument for estimating pesticide residues on 

plants. Environ Toxicol Chem 13(9):1383–1391. 

Kirkwood JK. 1983. Minireview. A limit to metabolisable energy intake in mammals and 

birds. Comp Biochem Physiol A 75(1):1-3. 

Martin, C. M., H. S. Zim, and A. C. Nelson. 1951. American Wildlife and Plants - A Guide 

to Wildlife Food Habits, Dover Publishers Inc., New York. 

Mineau, P., B.T. Collins, and A. Baril. 1996. On the use of scaling factors to improve 

interspecies extrapolation to acute toxicity in birds. Reg Toxicol Pharmacol 24:24–29. 

Urban, D.J. and Cook, N. 1986. Hazard Evaluation Division, Standard Evaluation Procedure: 

Ecological Risk Assessment 104.pp. Document Number No. PB 86 247 657. EPA-540/9-86-

167. 

USDA. 2002. 2002 Census of Agriculture. Available on-line at 

http://www.nass.usda.gov/Census_of_Agriculture/index.asp

U.S. EPA. 1993. Wildlife Exposure Factors Handbook. Volume I of II. EPA/600/R-93/187a. 

U.S. Environmental Protection Agency, Office of Research and Development, Washington, 

DC. 20460. 

U.S. EPA. 1999. ECOFRAM. U.S. Environmental Protection Agency, Washington, DC. 

Available on-line at http://www.epa.gov/oppefed1/ecorisk/index.htm. 

U.S. EPA. 2001. Ecological Risk Assessor Orientation Package. U.S. Environmental 

Protection Agency, Ecological Fate and Effects Division. Draft Version, August 2001. 

U.S. EPA. 2002a. Data Requirements for Registration. U.S. Environmental Protection 

Agency, Washington, DC. Code of Federal Regulations 40 CFR §158.202. 

U.S. EPA. 2002b. Guidance for Selecting Input Parameters in Modeling the Environmental 

Fate and Transport of Pesticides, Version II. U.S. Environmental Protection Agency, 

Washington, DC. February 28, 2002. 
63

U.S. EPA. 2004. Overview of Ecological Risk Assessment Process in the Office of Pesticide 

Programs, U.S. Environmental Protection Agency. Endangered and Threatened Species 

Effects Determinations. Office of Prevention, Pesticides, and Toxic Substances, Office of 

Pesticides Programs. Washington, DC. January 23, 2004. 

U.S. EPA. 2006a. User’s Guide for T-REX (Terrestrial Residue Exposure model) Version 

1.3.1 U.S. Environmental Protection Agency. Release December 7, 2006. 

U.S. EPA. 2006b. TerrPlant Terrestrial Plant Exposure Model. Version 1.2.2. U.S. 

Environmental Protection Agency. Released December 26, 2006. 
64

APPENDIX A. Environmental Fate Data 

161-1. Hydrolysis 

MRID 46800007,8 (Acceptable)

[ethyl-1-14C]-labeled 2-(4-chlorophenyl)-N-[2-(3-methoxy-4-prop-2-ynyloxy-phenyl)-ethyl]-

2-prop-2-ynyloxy-acetamide (mandipropamid; NOA446510; radiochemical purity 98.9%) 

was stable in pH 5, 7, and 9 sterile aqueous buffered solutions at 25 oC over the course of a 

32-day incubation period. Overall recoveries of [14C]residues averaged 100.0 ± 3.4% of the 

applied (range 94.4-104.9%) from the pH 5 buffer solution, 98.1 ± 0.8% of the applied (range 

97.2-99.4%) from the pH 7 buffer solution, and 100.1 ± 1.1% (range 99.1-101.6%) from the 

pH 9 buffer solution. There was no pattern of loss of material over time from any of the 

buffer solutions. [14C]Mandipropamid averaged 97.8-102.5% of the applied in the pH 5 

solutions, 97.5-99.0% in the pH 7 solutions, and 99.3-101.6% in the pH 9 solutions. No 

major or minor transformation products were detected; mandipropamid was the only 

compound detected and comprised 100% of the recovered at all sampling intervals. Volatiles 

were not measured. This study is classified as Acceptable. 

161-2. Aqueous Photolysis 

MRID 46800009(Acceptable)

[chlorophenyl-U-14C]-labeled 2-(4-chlorophenyl)-N-[2-(3-methoxy-4-prop-2-ynyloxyphenyl)-ethyl]-2-prop-2-ynyloxy-acetamide (mandipropamid; NOA446510; radiochemical 

purity >98%), at a nominal concentration of 1 μg a.i./mL, at 25°C in sterilized pond water 

from the UK (pH 7.02), degraded with a reviewer-calculated first-order linear half-life of 

15.2 hours based on the continuous irradiation of 44.79 W/m2 (300-400 nm); 1 hour of 

artificial light was equivalent to 0.65 hours of summer sunlight (68.98 W/m2; 300-400 nm) at 

40°N latitude. Mandipropamid was stable in the dark controls during the 7 days of 

incubation. In the irradiated buffer solutions, no major transformation products were 

identified. Polar compounds totaled a maximum average of 36.7% of the applied at 168 

hours posttreatment (individual samples 24.7% and 48.7%). Two minor nonpolar 

transformation products were identified. CGA380778 and NOA458422 averaged maximums 

of 3.7% and 3.9% of the applied, respectively. The study is Acceptable. 

MRID 46800010(Acceptable)

[methoxyphenyl-U-14C]-labeled 2-(4-chlorophenyl)-N-[2-(3-methoxy-4-prop-2-ynyloxyphenyl)-ethyl]-2-prop-2-ynyloxy-acetamide (mandipropamid; NOA446510; radiochemical 

purity >95.7%), at a nominal concentration of 1 μg a.i./mL, at 25°C in sterilized pond water 

from the UK (pH 7.02). degraded with a reviewer-calculated first-order linear half-life of 
65

15.2 hours based on the continuous irradiation of 22.4 hours, continuously irradiated using a 

filtered xenon lamp (300- 800 nm) for 166.4 hours (ca. 7 days). Mandipropamid was stable 

in the dark control during the 3 days of incubation. No major transformation products were 

isolated and no minor transformation products were identified in either the irradiated samples 

or dark controls. In the irradiated solutions only, unidentified polar compounds totaled a 

maximum of 25.0% of the applied at 72.2 hours posttreatment. This fraction consisted of at 

least 14 separate components with no single component >8.4% of the applied. At 72 hours 

posttreatment, 14CO2 averaged 6.0% of the applied in the irradiated samples and were not 

detected in the dark controls. Based on the study results, mandipropamid photodegrades to 

numerous minor polar compounds and CO2. The study is Acceptable. 

MRID 46800011,12(supplemental)

[chlorophenyl-U-14C]-labeled 2-(4-chloro-phenyl)-N-[2-(3-methoxy-4-prop-2-ynyloxyphenyl)-ethyl]-2-prop-2-ynyloxy-acetamide (mandipropamid; NOA446510) radiochemical 

purity 98.1%), at a nominal concentration of 1.0 mg a.i./L at 25°C sterile pH 7 buffer (0.01M 

phosphate), continuously irradiated using a filtered xenon lamp (290- 750 nm) for 15 days, 

dissipated with a half-life of 6.6 days (158.4 hours), based on the continuous irradiation of 

30.74 W/m2 (300-400 nm); 1 hour of artificial light was equivalent to 0.45 hours of summer 

sunlight (68.98 W/m2; 300-400 nm) at 40°N latitude. [14C]Mandipropamid was stable in the 

dark controls. No major transformation products were isolated from either the irradiated 

samples or dark controls. Based on the study results, mandipropamid photodegrades to 

numerous minor transformation products and CO2. This study is supplemental and 

upgradeable upon submission of the detailed results (concentration of parent) or the square 

vessel experiment. 

MRID 46800013,14(Acceptable)

[methoxyphenyl-U-14C]-labeled 2-(4-chloro-phenyl)-N-[2-(3-methoxy-4-prop-2-ynyloxyphenyl)-ethyl]-2-prop-2-ynyloxy-acetamide (mandipropamid; NOA446510; radiochemical 

purity >99%), at a nominal concentration of 1.0 mg a.i./L, at 25°C sterile pH 7 buffer (0.01M 

phosphate) continuously irradiated using a filtered xenon lamp (300- 800 nm) for 336 hours, 

dissipated with a half-life of 26.4 hours, based on the continuous irradiation of 29.93 W/m2 

(300-400 nm); 1 hour of artificial light was equivalent to 93 W/m2 (300-400 nm); 1 hour of 

artificial light was equivalent to 0.43 hours of summer sunlight (68.98 W/m2; 300-400 nm) at 

40°N latitude. No major transformation products were isolated from either the irradiated 

samples or dark controls. No minor transformation products were identified in the irradiated 

samples and none were isolated from the dark controls. In the irradiated buffer solution, 16 

minor nonpolar transformation products, none averaging >5% of the applied, and at least 10 

minor polar transformation products were isolated. 
66

161-3. Soil Photolysis 

MRID 46800015 (Acceptable)

[

14C-chlorophenyl]-labeled 2-(4-chlorophenyl)-N-[2-(3-methoxy-4-prop-2-ynyloxy-phenyl)-

ethyl]-2-prop-2-ynyloxy-acetamide (mandipropamid; NOA446510; radiochemical purity 

>98.0%) on loam soil (pH 7.1, organic matter 3.5%) from Switzerland under continuous 

irradiation for 15 days at 20 ± 2°C, degraded with a half-life of 16.39 days and 20.33 days in 

the irradiated samples for the dry soil and moist soil experiments, respectively. The intensity 

of the Xenon arc lamp was 53.14-53.98 W/m2

/nm, which was reported to be similar to 

natural summer sunlight at latitude 30-50°N. Mandipropamid degrades to CGA380778, 

NOA458442 and SYN521195. CGA380778 degrades to NOA459119 and CGA380775. 

NOA458442 degrades to CGA380775 and SYN505503. SYN521195 degrades to 

SYN505503. CGA380775 degrades to NOA459119. The transformation products are 

ultimately degraded to non-extractable residues and carbon dioxide. This study is acceptable. 

162-1. Aerobic Soil Metabolism 

MRID 46800020,21 (Acceptable)

[

14C-chlorophenyl]-labeled 2-(4-chlorophenyl)-N-[2-(3-methoxy-4-prop-2-ynyloxy-phenyl)-

ethyl]-2-prop-2-ynyloxy-acetamide (mandipropamid; NOA446510; radiochemical purity 

99.28%) was applied at the rate of 0.23 mg a.i./kg soil, equivalent to 150 g a.i./ha (nominal) 

to a sandy loam soil (pH 6.6, organic carbon 0.5%) from Visalia, California for 371 days 

under aerobic conditions in darkness at 25 ± 1°C and 75% field moisture capacity at 1/3 bar. 

The linear and nonlinear half-lives of [14C]mandipropamid in aerobic soil were 72.2 and 34.3 

days, respectively. No major transformation products were identified. Four minor 

transformation products identified: CGA380778 (benzeneacetamide, 4-chloro-alphahydroxy-N-[2-[3-methoxy-4-(2-propynyloxy)phenyl]ethyl]) was a maximum of 4.25% at 30 

days, CGA380775 (benzeneacetamide, 4-chloro-alpha-hydroxy-N-[2-(4-hydroxy-3-

methoxyphenyl)ethyl]) was a maximum of 0.51% at 30 days, SYN500003 was a maximum 

of 0.27% at 7 days, and NOA458422 was a maximum 0.18% at study termination. 

A supplementary study at a high dose was conducted in order to identify mandipropamid and 

transformation products. Mandipropamid was applied to soil at 1.35 mg a.i./ kg soil. The 

concentration of mandipropamid decreased from 97.25% of the applied at day 0 to 48.74% at 

59 days and was 6.69% at study termination. The first-order linear and nonlinear half-life 

values were 100.5 and 59.2 days, respectively, in the sandy loam soil. The major 

transformation product was volatilized 14CO2 totaling 43.1% of the applied. Four minor 

transformation products were identified as CGA380778, CGA380775, SYN500003 and 

NOA458422. 
67

A second supplementary study was performed to determine the microbial viability of the soil 

by monitoring for carbon dioxide efflux with a Micro-Oxymax Biomass Analyzer for ca. 18 

hours. The biomass of the soil samples after incubation for 0, 182 and 371 days was 124.07, 

62.32 and 44.43 mg C/kg soil, respectively. This study is acceptable. 

MRID 46800022 (Supplemental)

[methoxyphenyl-U-14C]-labeled 2-(4-chlorophenyl)-N-[2-(3-methoxy-4-prop-2-ynyloxyphenyl)-ethyl]-2-prop-2-ynyloxy-acetamide (mandipropamid, NOA 446510; radiochemical 

purity 98.9%} was studied in a silt loam soil (pH 7.2, organic carbon 2.14%) from 

Switzerland for 120 days under aerobic conditions in dark at 20.3 ± 0.3°C and 40% of water 

holding capacity at pF 1. [14C]Mandipropamid was applied at the rate of 0.40 mg a.i./kg soil, 

which is equivalent to 0.30 kg a.i./ha. Based on nonlinear analysis and using individual 

sample data, the half-life was determined to be 19.6 days. The first-order linear half-life was 

26.1 days. 

No major transformation products were isolated. The only minor transformation product that 

was identified was CGA380778 which averaged a maximum of 2.9% of the applied. 

Unidentified “Minor metabolites” (up to 13 compounds) totaled a maximum of 2.4%, and 

“remainder” (unresolved radioactivity in HPLC and Soxhlet extracts) was observed at a 

maximum of 8.7%. Extractable [14C] residues decreased from 96.79% of the applied at time 

0 to 9.07% at 120 days, while nonextractable [14C]residues increased to 45.45% at 120 days. 

At 120 days posttreatment, 14CO2 and organic volatiles accounted for 37.06% and 0.01% of 

the applied, respectively. This study is classified as supplemental and upgradeable upon 

submission of additional information related to classification of soils used in this study, in 

accordance to FAO Soil Classification (i.e. Soil Units) or equivalent U.S. Soil Taxonomy. 

MRID 46800023 (Supplemental)

The biotransformation of [14C-methoxyphenyl]-labeled 2-(4-chloro-phenyl)-2-hydroxy-N-[2-

(3-methoxy-4-prop-2-ynyloxy-phenyl)-ethyl]-acetamide (CGA380778; radiochemical purity 

97.9%) was studied in a silt loam soil (pH 7.35, organic carbon 2.2%) from Switzerland and 

a sandy clay loam soil (pH 5.88, organic carbon 2.7%) from the United Kingdom for 28 days 

and a sandy loam soil (pH 6.0, organic carbon 0.5%) from the United States for 120 days 

under aerobic conditions in darkness at 19.3 ± 0.5°C and soil moisture of pF2. 

[

14C]CGA380778 was applied at a rate of 0.09 mg a.i./kg, equivalent to 9 g a.i./ha (nominal). 

CGA380778 dissipated more slowly in the sandy loam soil compared to the silt loam and 

sandy clay loam soils. The linear and nonlinear half-lives of CGA380778 were 6.4 and 3.5 

days in the silt loam soil, 6.9 and 3.1 days in the sandy clay loam soil and 57.8 and 41.5 days 

in the sandy loam soil, respectively. One major transformation product was volatilized 14CO2

(identification confirmed) totaling means of 51.0%, 50.6% and 31.5% of the applied for the 

silt loam, sandy clay loam and sandy loam soils, respectively, at study termination; volatile 
68

[

14C]organic compounds were not detected (≤0.2%) for all three soils at any sampling 

interval. No minor transformation products were identified. 

This study is classified as supplemental and upgradeable upon submission additional 

information related to classification of soils used in this study, in accordance to FAO Soil 

Classification (i.e. Soil Units) or equivalent U.S. Soil Taxonomy. 

MRID 46800024,25 (Supplemental)

The biotransformation of [14C-methoxyphenyl]-labeled 2-(4-chlorophenyl)-N-[2-(3-methoxy4-prop-2-ynyloxy-phenyl)-ethyl]-2-prop-2-ynyloxy-acetamide (mandipropamid; 

NOA446510; radiochemical purity >97%) was studied in a sandy loam soil (pH 7.3, organic 

carbon 2.3%) from Switzerland for 119 days under aerobic conditions in darkness at 20 ±

2°C and 75% of pF2 moisture. Mandipropamid was applied at the rate of 0.2 mg a.i./kg soil 

and 1.0 mg a.i./kg soil (nominal). At the 0.2 mg a.i./kg application rate, the linear and 

nonlinear half-lives of mandipropamid were 77.9 and 77.0 days, respectively. Two minor 

transformation products, CGA380778 and SYN536638 (unknown 1) formed at maximums of 

1.4% (28 and 119 days) and 2.4% (91 days) of the applied, respectively. One transformation 

product, NOA458422, was detected by LC/MS/MS, but was below the limit of detection for 

HPLC. At study termination volatilized 14CO2 totaled 21.8% of the applied. 

At the 1.0 mg a.i./kg application rate, the linear and nonlinear half-lives of mandipropamid 

were 103.5 days. Two minor transformation products, CGA380778 and SYN536638 

(unknown 1) formed at maximums of 1.7% (7 days) and 3.1% (119 days) of the applied, 

respectively. Total extractable [14C]residues decreased from an average of 94.4% of the 

applied at day 0 to 49.2% at study termination, while nonextractable [14C]residues increased 

from 1.3% of the applied at day 0 to 27.1% at study termination. At study termination, 

volatilized 14CO2 totaled 19.7% of the applied. 

Mandipropamid is ultimately degraded into carbon dioxide and unextractable residues. 

Two supplementary studies were performed with soil samples treated with 0.2 mg a.i./kg 

mandipropamid maintained at low moisture (30% of pF2 moisture) and at low temperature 

(10°C) for 119 days. Mandipropamid degraded more slowly in the supplementary 

experiments. In the low moisture study, the concentration of mandipropamid decreased from 

an average of 92.6% of the applied at day 0 to 53.7% at study termination. The calculated 

DT50 and DT90 were 149.5 and 497.2 days, respectively, based on both simple first-order 

regression, and first-order multi-compartment regression. The same transformation products, 

CGA380778 and SYN536638 (unknown 1), were detected in each study at ≤1.7% of the 

applied. 

This study is classified as supplemental and upgradeable upon the submission of additional 

information related to classification of soils used in this study, in accordance to FAO Soil 

Classification (i.e. Soil Units) or equivalent U.S. Soil Taxonomy. 
69

MRID 46800027 (Supplemental)

The biotransformation of [chlorophenyl-U-14C]-labeled 2-(4-Chlorophenyl)-N-[2-(3-

methoxy-4-prop-2-ynyloxy-phenyl)-ethyl]-2-prop-2-ynyloxy-acetamide (mandipropamid, 

NOA446510, radiochemical purity 100%} was studied in a loam/silt loam soil (pH (KCl) 

7.3, organic carbon 1.7%) from Switzerland for 120 days under aerobic conditions in dark at 

19.0 ± 0.6°C and soil moisture content of 100% of pF 2. [14C]Mandipropamid was applied at 

the rate of 0.40 mg a.i./kg soil, which is equivalent to 0.30 kg a.i./ha. The nonlinear analysis 

(SigmaPlot v 9) and using individual sample data, the half-life was determined to be 26.1 

days. The first-order linear half-life was 32.4 days. No major transformation products were 

isolated. The only minor transformation product that was identified was CGA380778, which 

averaged a maximum of 3.2% of the applied. Nine minor transformation products totaled a 

maximum of 2.4% of the applied and “remainder” (unresolved radioactivity) was observed at 

a maximum of 11.4%. At 120 days posttreatment, [14C]CO2 and organic volatiles accounted 

for 36.0% and 0.0% of the applied, respectively. 

Based on the study results, mandipropamid degrades into multiple minor metabolites, 

including CGA380778, CO2, and tightly bound residues. 

This study is classified as as supplemental and upgradeable upon the submission of 

additional information related to classification of soils used in this study, in accordance to 

FAO Soil Classification (i.e. Soil Units) or equivalent U.S. Soil Taxonomy. 

MRID 46800028 (Supplemental)

The biotransformation of [14-C-chlorophenyl]-labeled 2-(4-chlorophenyl)-N-[2-(3-methoxy4-prop-2-ynyloxy-phenyl)-ethyl]-2-prop-2-ynyloxy-acetamide (mandipropamid; 

NOA446510; radiochemical purity >98.7%) was studied in a sandy clay loam soil (pH 6.2, 

organic carbon 3.5%) from the United Kingdom, a loamy sand soil (pH 6.5, organic carbon 

0.8%) from Germany and a loam soil (pH 8.5, organic carbon 1.3%) from France for 120 

days under aerobic conditions in darkness at 20 ± 2°C and pF2 moisture. Mandipropamid 

was applied at the rate of 0.2 mg a.i./kg soil (nominal). 

In sandy clay loam soil, based on first-order linear and nonlinear regression analysis, 

mandipropamid degraded with half-life values of 51.3 and 43.9 days, respectively. 

In loamy sand soil, based on first-order linear and nonlinear regression analysis, 

mandipropamid degraded with half-life values of 83.5 and 80.6 days, respectively. 

In loam soil, based on first-order linear and In sandy clay loam soil, based on first-order 

linear (Excel 2003) and nonlinear (SigmaPlot v 9) regression analysis, mandipropamid 

degraded with half-life values of 51.3 and 43.9 days, respectively (DER Attachment 2). 

Observed DT50 value was 21-28 days (Table 9, p. 51). Using Model Manager v. 1.1, the 

study author determined the half-life for mandipropamid using simple first order and first 
70

order multicompartment kinetics as 43.9 and 33.7 days, respectively (p. 26, Table 8, p. 50, 

Appendix 7, p. 40 and Figure 29-30, pp. 116-117). 

In loamy sand soil, based on first-order linear and nonlinear regression analysis, 

mandipropamid degraded with half-life values of 83.5 and 80.6 days, respectively. 

In loam soil, based on first-order linear and nonlinear regression analysis, mandipropamid 

degraded with half-life values of 90.0 and 85.6 days, respectively. In each of the soils, one 

minor transformation product was identified as CGA380778. LC/MS/MS analysis identified 

low levels of transformation products not identified by HPLC and 2D-TLC including: 

CGA380775, NOA458422 and SYN505503. Mandipropamid is ultimately degraded into 

carbon dioxide and bound residues. This study is classified as as supplemental and 

upgradeable upon the submission of additional information related to classification of soils 

used in this study, in accordance to FAO Soil Classification (i.e. Soil Units) or equivalent 

U.S. Soil Taxonomy. 

162-2 Anaerobic Soil Metabolism 

MRID 46800027 (Supplemental)

The biotransformation of [chlorophenyl-U-14C]-labeled 2-(4-chlorophenyl)-N-[2-(3-

methoxy-4-prop-2-ynyloxy-phenyl)-ethyl]-2-prop-2-ynyloxy-acetamide (mandipropamid, 

NOA446510, radiochemical purity 100%} was studied in flooded loam/silt loam soil (pH 

(KCl) 7.3, organic carbon 1.7%) from Switzerland for 120 days under anaerobic conditions 

in dark at 19.0 ± 0.6°C. [14C]Mandipropamid was applied at the rate of 0.40 mg a.i./kg soil, 

which is equivalent to 0.30 kg a.i./ha. Anaerobicity, temperature and other experimental 

conditions were reportedly maintained throughout the study. In the water layer, the dissolved 

oxygen and pH levels were 0.01-0.96 mg/L and 6.50-8.77, respectively. Redox potentials in 

the water layer ranged from −148 to +68 mV; redox potentials in the soil ranged −232 to +72 

mV. The viability of the soil microflora in soil treated with mandipropamid was not 

determined. 

Based on first-order linear regression analysis, mandipropamid dissipated with a half-life of 

198.0 days. Based on nonlinear analysis, the half-life was 183 days. 

No major transformation products were isolated. The only minor transformation product that 

was identified was CGA380778, which averaged a maximum of 3.9% of the applied. Nine 

minor transformation products totaled a maximum of 4.1% of the applied and “remainder” 

(unresolved radioactivity) was observed at a maximum of 9.6%. At 120 days postflooding, 

the nonextractable residues were partitioned into 3.1-6.5% of the applied as fulvic acids, 1.3-

5.6% humic acids and 16.7-25.2% humin. At 120 days postflooding, 14CO2 and organic 

volatiles accounted for 17.4% and 0.2%, respectively. Based on the study results, 

mandipropamid degrades into multiple minor metabolites, including CGA380778, CO2, and 

tightly bound residues. This study is classified as supplemental and upgradeable upon the 

submission of additional information related to classification of soils used in this study, in 

accordance to FAO Soil Classification (i.e. Soil Units) or equivalent U.S. Soil Taxonomy. 
71

162-3 Anaerobic Aquatic Metabolism 

MRID 46800033,34 (Unacceptable)

The biotransformation of [methoxyphenyl-U-14C]-labeled 2-(4-chloro-phenyl)-N-[2-(3-

methoxy-4-prop-2-ynyloxy-phenyl)-ethyl]-2-prop-2-ynyloxy-acetamide (mandipropamid, 

NOA446510; radiochemical purity ≥98.0%) was studied in lake water-silt loam sediment 

(water pH 8.1-8.25, dissolved organic carbon 12.1 mg/L; sediment pH 7.2-7.6, organic 

carbon 5.5%) and lake water-loamy sand sediment (water pH 5.8-5.83, dissolved organic 

carbon 1.5 mg/L; sediment pH 4.6-5.3, organic carbon 0.9%) systems from the United 

Kingdom for 120 days under anaerobic conditions in darkness at 20 ± 2°C. Based on the 

water volume, [14C]mandipropamid was applied at a rate of 0.26 mg a.i./L. For both 

systems, the sediment:water ratio used was 1:4 (40 g dry wt. sediment:160 g water). 

The test conditions presented in the study appear to have been maintained throughout the 

120-day incubations. In untreated lake water-silt loam systems incubated alongside the 

treated systems, conditions were moderately reducing to moderately oxidizing in the water 

layers and moderately reducing in the sediment with average redox potentials of +253 ± 79 

mV and +124 ± 15 mV, respectively, and water pH levels of 8.24 ± 0.15. In untreated lake 

water-loamy sand systems, conditions in the water layers and sediment went from 

moderately reducing during the initial month posttreatment to moderately oxidizing from 2 

months to study termination with average redox potentials in the water layer and sediment 

increasing from +78 ± 14 mV at 6 days posttreatment to +231 ± 10 mV at 59 days and were 

+229 ± 7 mV at 119 days; water pH levels averaged 7.51 ± 0.33 over the 120-day incubation. 

For both systems, the following four transformation products were detected: 

• 2-(4-chloro-phenyl)-N-[2-(3-hydroxy-4-prop-2-ynyloxy-phenyl)-ethyl]-2-prop-2-

ynyloxy-acetamide (SYN521195), 

• N-[2-(4-allyloxy-3-hydroxy-phenyl)-ethyl]-2-(4-chloro-phenyl)-2-prop-2-ynyloxyacetamide (SYN539678), 

• 2-allyloxy-N-[2-(4-allyloxy-3-hydroxy-phenyl)-ethyl]-2-(4-chloro-phenyl)-acetamide 

(SYN539679) and 

• N-[2-(4-allyloxy-3-methoxy-phenyl)-ethyl]-2-(4-chloro-phenyl)-2-prop-2-ynyloxyacetamide (SYN536638). 

SYN521195 and SYN539678 were major transformation products in the lake water-silt loam 

systems, but minor products in the lake water-loamy sand systems. SYN539679 and 

SYN536638 were minor products in both systems. Dissipation of mandipropamid and 

formation of products in the total system occurred at a faster rate in the silt loam systems as 

compared to the loamy sand systems. The faster dissipation rate in the silt loam systems may 

have been due to greater microbial activity, with microbial biomass (as μC/g soil) ca. 5- to 

10-fold higher in the silt loam systems as compared to the loamy sand systems. 14CO2 was a 

major volatile product with maximum totals of 40.3% and 36.0% of the applied at study 

termination for the lake water-silt loam and lake water-loamy sand systems, respectively, 
72

while no [14C]residues were extracted from the 7- to 3-day organic volatiles carbon traps. 

Mandipropamid in the total system decreased from 96.3% of the applied at day 0 to 58.2% at 

21days, 41.3% at 30 days, 9.5% at 62 days, 2.3-2.4% at 83-100 days and was 0.1% at study 

termination; 120-day sediment extracts were not analyzed. In the water layer, 

mandipropamid decreased from 93.6% at day 0 to 51.8% at 21 days, 38.7% at 30 days, 9.5% 

at 62 days, 1.4% at 100 days and was 0.1% at 120 days. In the sediment, 

[

14C]mandipropamid increased from 2.7% at day 0 to 7.3% at 14 days, then decreased to 

2.6% at 30 days and was ≤1.1% at 42-100 days. Observed DT50 values were 21-30 days in 

the water layer, sediment and total system. Calculated linear half-lives (r2 = 0.4053-0.9473) 

were 14 days in the water layer and total system and 13 days in the sediment, while nonlinear 

half-lives (r2 = 0.9406-0.9861) were 22 days in the water and total system and 12 days in the 

sediment. Maximum levels of the transformation products in the water, sediment and total 

system were as follows: 2.8%, 5.6% and 8.5%, respectively, for SYN521195, 2.1%, 6.4% 

and 6.4%, respectively, for SYN539678, and 3.3%, 2.3% and 4.0%, respectively, for 

SYN539679/SYN536638. Unretained [14C]residues were detected at maximums of 10.4%, 

5.5% and 15.5% in the water, sediment and total system, respectively. In a supplementary 

experiment, volatilized 14CO2 (2M KOH) and volatile [14C]organic compounds (combustion 

furnace/2M KOH) totaled 23.29% and 8.55% of the applied, respectively, after 40 days of 

anaerobic incubation of [methoxyphenyl-U-14C]mandipropamid treated lake water-silt loam 

systems. Based on these results, the study author proposed that the incomplete material 

balances in this study were due to untrapped low molecular weight organic volatiles, such as 

methane. This study is classified as unacceptable for the following reasons: 

• For both systems, material balances were incomplete with up to 46.4% and 40.0% of 

the applied unaccounted for in the lake water-silt loam and lake water-loamy sand 

systems, respectively. 

• For both systems, all transformation products detected at ≥10% of the applied may 

not have been identified. 

162-4 Aerobic Aquatic Metabolism 

MRID 46800030,31 (Supplemental)

The biotransformation of [chlorophenyl-U-14C]-labeled 2-(4-chloro-phenyl)-N-[2-(3-

methoxy-4-prop-2-ynyloxy-phenyl)-ethyl]-2-prop-2-ynyloxy-acetamide (mandipropamid, 

NOA446510; radiochemical purity ≥98.6%) was studied in lake water-silt loam sediment 

(water pH 7.63-7.84, dissolved organic carbon <2.0 mg/L; sediment pH 7.0-7.2, organic 

carbon 5.8%) and lake water-sand sediment (water pH 6.48-6.68, dissolved organic carbon 

9.3 mg/L; sediment pH 4.9-5.3, organic carbon 0.5%) systems from the United Kingdom for 

100 days under aerobic conditions in darkness at 20 ± 2°C. For both systems, the 

sediment:water ratio used was 1:4 (45 g dry wt. sediment:180 g water). Sediment and water 

were pre-incubated for 13-15 days, then following treatment, duplicate vessels per system 

type were collected after 0, 1, 2, 3, 10, 30, 45, 70 and 100 days of incubation; however, only 

one of the two replicates per system type was processed and analyzed at the 2- and 3-day 
73

intervals. Water layers were separated from the sediment via aspiration and analyzed 

directly. Sediment samples were extracted either once (0-day sediments) or twice (all 

remaining sediment samples) with acetonitrile; resulting extracts were concentrated 

(method/conditions not reported. 

The test conditions presented in the study appear to have been maintained throughout the 

incubations. In untreated lake water-silt loam systems incubated alongside the treated 

systems, conditions were moderately oxidizing in the water layers and moderately reducing 

in the sediment with average redox potentials of +280 ± 25 mV and +112 ± 11 mV, 

respectively, and dissolved oxygen and pH levels of 3.3 ± 0.2 mg/L and 7.23 ± 0.74, 

respectively, in the water. In untreated lake water-sand systems, conditions were strongly 

oxidizing in the water layers and moderately to strongly oxidizing in the sediment with 

average redox potentials of +485 ± 30 mV and +392 ± 22 mV, respectively, and dissolved 

oxygen and pH levels of 4.0 ± 0.0 mg/L and 4.92 ± 0.16, respectively, in the water. 

For both systems, the following six transformation products were detected: 

• SYN500003 (chemical name not provided), 

• SYN504851 (chemical name not provided), 

• SYN539678 (N-[2-(4-allyloxy-3-hydroxy-phenyl)-ethyl]-2-(4-chloro-phenyl)-2-prop2-ynyloxy-acetamide), 

• SYN539679 (2-allyloxy-N-[2-(4-allyloxy-3-hydroxy-phenyl)-ethyl]-2-(4-chlorophenyl)-acetamide), 

• SYN536638 (N-[2-(4-allyloxy-3-methoxy-phenyl)-ethyl]-2-(4-chloro-phenyl)-2-

prop-2-ynyloxy-acetamide) and 

• SYN521195 (2-(4-chloro-phenyl)-N-[2-(3-hydroxy-4-prop-2-ynyloxy-phenyl)-ethyl]-

2-prop-2-ynyloxy-acetamide). 

SYN504851 was a major transformation product, while SYN500003, SYN539678, 

SYN539679, SYN536638 and SYN521195 were minor products. Dissipation of 

mandipropamid and formation of products in the total system occurred at a faster rate in the 

silt loam systems as compared to the sand systems. The faster dissipation rate in the silt loam 

systems may have been due to greater microbial activity, with microbial biomass (as μC/g 

soil) 10-fold higher in the silt loam systems as compared to the sand systems. Additionally, 

after application of [14C]mandipropamid to the water layers, [14C]residues readily partitioned 

from the water layer to the silt loam sediment, with movement from the water layer to the 

sand sediment occurring at a slower rate. 

MRID 46800032 (Unacceptable)

The biotransformation of [chlorophenyl-U-14C]- and [methoxyphenyl-U-14C]-labeled 2-(4-

chloro-phenyl)-N-[2-(3-methoxy-4-prop-2-ynyloxy-phenyl)-ethyl]-2-prop-2-ynyloxyacetamide (mandipropamid; NOA446510; radiochemical purities 99.1%) was studied in a 

simulated pond water-sandy clay loam sediment (water pH 7.91, total organic carbon 5.6 
74

mg/L; sediment pH 7.2-7.7, organic carbon 1.9%) system from the United Kingdom for 120 

days under natural, outdoor conditions. Based on the water volume, [14C]mandipropamid 

was applied at a rate of 0.06-0.07 mg a.i./L. The sediment:water ratio used was ca. 1:3 (ca. 

10-cm sediment layer:30-cm water layer); the water volume was ca 648 L, but sediment 

weight/volume was not reported. 

For both systems, conditions were moderately reducing in the water layers and reducing to 

strongly reducing in the sediments during the initial month posttreatment, after which redox 

potentials were not measured. Redox potentials in the water layers decreased from +177.7 to 

+199.2 mV at 3 days to −5.6 to 11.9 mV at 17-31 days, while in the sediment were −160.1 to 

−324.4 mV at 3-17 days and −84.2 to −80.6 mV at 31 days. 

Observed DT50 values for mandipropamid (both labels) were 2-7 days in the water layer and 

total system and 7-15 days in the sediment. In the water, sediment and total system, 

calculated linear half-lives (r2 = 0.6742-0.9818) were 4, 39 and 21 days, respectively, with 

nonlinear half-lives (r2

 = 0.7428-0.8769) of 4, 11 and 7 days, respectively. 

SYN504851 was a major transformation product, with SYN521195 a major product in the 

chlorophenyl-label treated system and neared 10% of applied in the methoxyphenyl-label 

treated system. SYN539678, SYN539679, SYN536638 and SYN500003 were minor 

products. In the chlorophenyl-label treated system, SYN521195 was detected at a maximum 

mean 10.8% of applied in the sediment and total system at 15 days, decreasing to 2.5% at 

study termination, and was only detected at one interval in the water at 1.1%; while in the 

methoxyphenyl-label treated system, SYN521195 was detected only in the sediment at a 

maximum mean 8.8% (range 7.9-9.6%). SYN504851 was detected at maximum means of 

7.2% (120 days), 4.5% (71 days) and 11.1% (120 days) in the water, sediment and total 

system, respectively. SYN500003 was detected at maximum means of 5.4%, 1.7% and 6.4% 

in the water, sediment and total system, respectively. SYN539678, SYN539679 and 

SYN536638 were detected only in the sediment (both labels) at maximum means of 5.6-

6.9%, 0.6-0.9% and 1.1-1.9%, respectively. Unidentified [14C]residues 

(unassigned/unaccounted for organo-and aqueous-soluble residues) were detected at 

maximums of 7.2-7.7%, 2.0-3.3% and 8.7-9.0% of the applied in the water, sediment and 

total system, respectively. Extractable [14C]residues (both labels) increased from means of 

5.6-7.7% of the applied at 1 hour to maximum means of 24.7-31.8% at 15 days, then 

decreased to 6.8-14.9% at 120 days. Nonextractable chlorophenyl-label [14C]residues 

increased from a mean 0.6% at day 0 (1 and 6 hours) to 27.1% at 120 days, while 

methoxyphenyl-label residues increased from 0.3-0.7% at day 0 to 29.2% at 71 days and 

were 20.2% at study termination. [14C]Residues (both labels) in the plant material comprised 

only 1.3-5.0% of the applied. In a supplemental experiment investigating the distribution 

depth of residues in the sediment, [14C]residues were found primarily in the upper 0- to 5-cm 

sediment layer; quantitative results were not reported. This study is classified as unacceptable 

for the following reasons: 
75

• Material balances were incomplete with up to 58.6% and 71.8% of the applied 

unaccounted for in the chlorophenyl- and methoxyphenyl-label treated systems, 

respectively. 

• The systems were not maintained at a constant temperature between 18 and 30°C. 

• The systems were not maintained in continuous darkness. 

163-1 Adsorption/Desorption 

MRID 46800035 (Supplemental)

The adsorption/desorption characteristics of [chlorophenyl-U-14C]-labeled 2-(4-chlorophenyl)-N-[2-(3-hydroxy-4-prop-2-ynyloxy-phenyl)-ethyl]-2-prop-2-ynyloxy-acetamide 

(SYN521195) were studied in a silt loam soil [pH 7.6, organic carbon 2.0%] from 

Switzerland, a silt loam soil [pH 7.9, organic carbon 0.8%] from France, and a sandy loam 

soil [pH 6.0, organic carbon 0.5%] from the United States, in a batch equilibrium experiment. 

The experimental temperature employed during the study was reported to be maintained at 

19.3 ± 0.04°C. The pH of the test solutions after adsorption ranged from 6.89-7.33 

After 48 hours of equilibration, 23.1-61.1%, 27.9-46.6%, and 17.7-36.4% of the applied 

[

14C]SYN521195 was adsorbed to the Gartenacker silt loam, Marsillargues silt loam, and 

Visalia sandy loam soils, respectively (reviewer-calculated). The Freundlich adsorption K 

values were 31.0, 9.2, and 2.83 for the Gartenacker silt loam, Marsillargues silt loam, and 

Visalia sandy loam soils, respectively; corresponding Freundlich Koc values were 1537, 1145, 

and 567. The Freundlich desorption K values were 161.2, 49.95, and 3.34 for the 

Gartenacker silt loam, Marsillargues silt loam, and Visalia sandy loam soils, respectively; 

corresponding Freundlich desorption Koc values were 7979, 6244, and 668. This study is 

classified as supplemental and upgradeable upon the submission of additional information 

related to classification of soils used in this study, in accordance to FAO Soil Classification 

(i.e. Soil Units) or equivalent U.S. Soil Taxonomy. The study was conducted using three 

soils, and only two soil types were represented. Additional study with a fourth soil is needed 

fourth soil as required by the Subdivision N, Chemistry: Environmental Fate, Section 163-1 

MRID 46800036 (Supplemental)

The adsorption/desorption characteristics of [chlorophenyl-U-14C]-labeled SYN539678 were 

studied in a loam soil [pH 7.1, organic carbon 2.0%] from Switzerland, a loam soil [pH 7.8, 

organic carbon 0.58%] from France, and a sandy loam soil [pH 6.0, organic carbon 0.47%] 

from California, in a batch equilibrium experiment. The equilibrating solution used was 

0.01M CaCl2 solution with a soil solution ratio of 1:39 (w:v) for all soils. All samples were 

prepared in duplicate. A desorption phase was not conducted. 
76

After 3 or 24 hours of equilibration, 7.6-8.9%, 15.0-23.2%, and 2.6-15.3% of the applied 

[

14C]SYN539678 was adsorbed to the Gartenacker loam, Marsillargues loam, and Visalia 

sandy loam soils, respectively. The adsorption K values were 10.57, 12.68, and 6.17 for the 

Gartenacker loam, Marsillargues loam, and Visalia sandy loam soils, respectively; 

corresponding Koc values were 520, 2200, and 1300. The Freundlich adsorption K values 

were 8.77, 11.96, and 9.19 for the Gartenacker loam, Marsillargues loam, and Visalia sandy 

loam soils, respectively; corresponding Freundlich Koc values were 430, 2100, and 2000. This 

study is classified as unacceptable because a desorption phase was not conducted for the 

degradates. 

MRID 46800037 (Supplemental) 

The adsorption/desorption characteristics of [phenyl-U-14C]-labeled (4-chloro-phenyl)-prop2-ynyloxy-acetic acid (SYN500003) were studied in a silt loam soil [Gartenacker, pH 7.6, 

organic carbon 2.0%] from Switzerland, a silt loam soil [Marsillargues, pH 7.9, organic 

carbon 0.8%] from France, and a sandy loam soil [Visalia, pH 6.0, organic carbon 0.5%] 

from the United States, in a batch equilibrium experiment. The adsorption phase of the study 

was carried out by equilibrating air-dried soil with [14C]SYN500003 at nominal test 

concentrations of 0.01, 0.05, 0.10, 0.50, and 1.00 mg a.i./kg soil, in the dark at 19.4 ± 0.1°C 

for 48 hours. The equilibrating solution used was 0.01M CaCl2 solution with a soil solution 

ratio of 1:1 (w:v) for all soils. The desorption phase of the study was carried out by replacing 

the adsorption solution with an equivalent volume of 0.01M CaCl2 solution and equilibrating 

in the dark at 19.4 ± 0.1°C for 24 hours. A single desorption step was conducted for all soils. 

The experimental temperature employed during the study was reported to be maintained at 

19.4 ± 0.1°C. The pH of the test solutions after adsorption ranged from 7.10-7.75. After 

desorption, the pH ranged from 6.74-6.85. 

After 48 hours of equilibration, 0.0-6.1%, 18.2-27.0%, and 1.4-30.0% of the applied 

[

14C]SYN500003 was adsorbed to the Gartenacker silt loam, Marsillargues silt loam, and 

Visalia sandy loam soils, respectively. The Freundlich adsorption K values were 0.06, 0.23, 

and 0.01 for the Gartenacker silt loam, Marsillargues silt loam, and Visalia sandy loam soils, 

respectively; corresponding Freundlich Koc values were 2.92, 19.79, and 2.89. The 

adsorption K and Koc values were not reported. The Freundlich desorption K values were 

0.08, 0.38, and 0.04 for the Gartenacker silt loam, Marsillargues silt loam, and Visalia sandy 

loam soils, respectively; corresponding Freundlich desorption Koc values were 3.88, 32.52, 

and 8.66. The desorption K and Koc values were not reported. This study is classified as 

supplemental and upgradeable upon the submission of additional information related to 

classification of soils used in this study, in accordance to FAO Soil Classification (i.e. Soil 

Units) or equivalent U.S. Soil Taxonomy. Additional study with a fourth soil is needed as 

required by Subdivision N, Chemistry: Environmental Fate, Section 163-1. 
77

MRID 46800038, 39 (Supplemental)

The adsorption/desorption characteristics of [methoxyphenyl-U-14C]-labeled 2-(4-

chlorophenyl)-N-[2-(3-methoxy-4-prop-2-ynyloxy-phenyl)-ethyl]-2-prop-2-ynyloxyacetamide (mandipropamid; NOA446510) were studied in a loam/silt loam soil [pH 7.1, 

organic carbon 2.6%] and a silt loam soil [pH 7.2, organic carbon 5.0%], each from 

Switzerland, a loamy sand soil [pH 5.1, organic carbon 1.0%] from Germany, and a silty clay 

loam soil [pH 7.3, organic carbon 1.2%] from France, in a batch equilibrium experiment. 

The adsorption phase of the study was carried out by equilibrating air-dried soil with 

[

14C]mandipropamid at nominal test concentrations of 0.16, 0.81, 1.61, 3.23, and 8.06 mg 

a.i./kg soil (loam/silt loam); 0.06, 0.30, 0.60, 1.20, and 3.0 mg a.i./kg soil (loamy sand); 0.08, 

0.40, 0.79, 1.59, and 3.97 mg a.i./kg soil (silty clay loam); and 0.25, 1.25, 2.5, 5.0, and 12.5 

mg a.i./kg soil (silt loam), in the dark at 20.3 ± 0.3°C for 24 hours. The equilibrating solution 

used was 0.01M CaCl2 solution with a soil solution ratio of 3.1:50 (w:v; loam/silt loam); 

8.3:50 (w:v; loamy sand); 6.3:50 (w:v; silty clay loam); and 2.0:50 (w:v; silt loam). The 

desorption phase of the study was carried out by replacing the adsorption solution with an 

equivalent volume of 0.01M CaCl2 solution and equilibrating in the dark at 20.3 ± 0.3°C for 

24 hours. Two desorption steps were performed for each test soil. The experimental 

temperature employed during the study was reported to be maintained at 20.3 ± 0.3°C. The 

pH of the test solutions during the study was not reported. After 24 hours of equilibration, 

65.0-93.8%, 77.1-100.8%, 60.8-81.9%, and 69.5-80.6% of the applied [14C]mandipropamid 

was adsorbed to the Gartenacker loam/silt loam, Borstel loamy sand, Marsillargues silty clay 

loam, and Vetroz silt loam soils. The Freundlich adsorption K values were 20.3, 12.9, 12.6, 

and 53.2 for the Gartenacker loam/silt loam, Borstel loamy sand, Marsillargues silty clay 

loam, and Vetroz silt loam soils, respectively; corresponding Freundlich Koc values were 782, 

1294, 1067, and 1064. The adsorption K and Koc values were not reported. Following the 

second desorption step, the percent of [14C]mandipropamid desorbed from the test soils, as 

percent of the radioactivity adsorbed, was 30.8-46.9% for the Gartenacker loam/silt loam, 

25.4-36.0% for the Borstel loamy sand, 19.5-36.3% for the Marsillargues silty clay loam, and 

30.9-38.9% for the Vetroz silt loam soil. The Freundlich desorption K values were 32.9, 

20.8, 21.7, and 86.8 for the Gartenacker loam/silt loam, Borstel loamy sand, Marsillargues 

silty clay loam, and Vetroz silt loam soils, respectively; corresponding Freundlich desorption 

Koc values were 1271, 2076, 1836, and 1736. The desorption K and Koc values were not 

reported. This study is classified as supplemental and upgradeable upon the submission of 

additional information related to classification of soils used in this study, in accordance to 

FAO Soil Classification (i.e. Soil Units) or equivalent U.S. Soil Taxonomy. Additional study 

with a fourth soil is needed as required by Subdivision N, Chemistry: Environmental Fate, 

Section 163-1. 
78

MRID 46800040, 41 (Supplemental)The adsorption/desorption characteristics of 

[methoxyphenyl-U-14C]-labeled 2-(4-chlorophenyl)-N-[3-methoxy-4-(prop-2-

ynyloxy)phenylethyl]-2-(prop-2-ynyloxy)acetamide (mandipropamid; NOA446510) were 

studied in a sandy loam soil [pH 6.6, organic carbon 0.52%] from California, a loamy sand 

soil [pH 4.9, organic carbon 0.70%] from Georgia, and a loamy sand soil [pH 6.7, organic 

carbon 1.16%] from New York, in a batch equilibrium experiment. The adsorption phase of 

the study was carried out by equilibrating air-dried soil with [14C]mandipropamid at nominal 

test concentrations of 0.05, 0.25, 0.50, 1.00, and 3.00 mg a.i./kg soil (Sanger sandy loam); 

0.05, 0.23, 0.45, 0.90, and 2.70 mg a.i./kg soil (Chula loamy sand); and 0.07, 0.37, 0.74, 

1.47, and 4.41 mg a.i./kg soil (North Rose loamy sand), in the dark at 19.4 ± 0.2°C for 24 

hours. The equilibrating solution used was 0.01M CaCl2 solution with a soil solution ratio of 

10.0:50 (w:v; Sanger sandy loam); 11.1:50 (w:v; Chula loamy sand); and 6.8:50 (w:v; North 

Rose loamy sand). The experimental temperature employed during the study was reported to 

be maintained at 19.4 ± 0.2°C; supporting data were not provided. The pH of the test 

solutions after adsorption ranged from 5.01 to 7.08. The pH of the test solutions ranged from 

6.16 to 7.03 at the first desorption step (one desorption step for all test concentrations except 

high-dose), 6.14 to 7.03 during the second desorption step (high dose only), and from 6.01 to 

7.08 during the third desorption step (high dose only). After 24 hours of equilibration, 47.2-

71.0%, 46.3-72.0%, and 55.7-91.4% of the applied [14C]mandipropamid was adsorbed to the 

Sanger sandy loam, Chula loamy sand, and North Rose loamy sand soils, respectively. The 

Freundlich adsorption K values were 3.68, 2.88, and 7.37 for the Sanger sandy loam, Chula 

loamy sand, and North Rose loamy sand soils, respectively; corresponding Freundlich Koc 

values were 693.9, 405.1, and 624.3. The adsorption K and Koc values were not reported. 

Following the first desorption step, the percent of [14C]mandipropamid desorbed from the 

test soils, as percent of the radioactivity adsorbed, was 21.4-40.1% for the Sanger sandy 

loam, 19.2-40.9% for the Chula loamy sand, and 21.9-34.9% for the North Rose loamy sand. 

Following the third desorption step, the percent of [14C]mandipropamid desorbed from the 

high-dose soils was 69.3%, 68.0%, and 63.2% for the Sanger sandy loam, Chula loamy sand, 

and the North Rose loamy sand soils, respectively (reviewer-calculated). The Freundlich 

desorption K values were 4.98, 4.33, and 11.86 for the Sanger sandy loam, Chula loamy 

sand, and North Rose loamy sand soils, respectively; corresponding Freundlich desorption 

Koc values were 939.6, 609.9, and 1004.8. For the high-dose soils following the third 

desorption step, Freundlich desorption K values were 2.39, 1.63, and 4.13 for the Sanger 

sandy loam, Chula loamy sand, and North Rose loamy sand soils, respectively; 

corresponding Freundlich desorption Koc values were 423, 229, and 229. The desorption K 

and Koc values were not reported for any of the test soils. This study is classified as 

supplemental and upgradeable upon the submission of additional information related to 

classification of soils used in this study, in accordance to FAO Soil Classification (i.e. Soil 

Units) or equivalent U.S. Soil Taxonomy. The study was conducted using three soils, and 

only two soil types were represented. Additional study with a fourth soil is needed as 

required by the Subdivision N, Chemistry: Environmental Fate, Section 163-1 
79

MRID 46800042, 43 (Supplemental)

The adsorption/desorption characteristics of [methoxyphenyl-U-14C]-labeled 2-(4-chlorophenyl)-2-hydroxy-N-[2-(3-methoxy-4-prop-2-ynyloxy-phenyl)-ethyl]acetamide 

(CGA380778) were studied in a sandy clay loam soil [pH 5.6, organic carbon 3.25%] from 

the United Kingdom, a loam soil [pH 7.2, organic carbon 2.06%] from Switzerland, and a 

sandy loam soil [pH 6.3, organic carbon 0.46%] from the United States, in a batch 

equilibrium experiment. The adsorption phase of the study was carried out by equilibrating 

air-dried soil with [14C]-CGA380778 at actual concentrations of 0.23, 0.61, 1.18, 6.19, and 

11.85 mg a.i./kg soil (18 Acres sandy clay loam and Gartenacker loam); and 0.11, 0.31, 0.59, 

3.09, and 5.93 mg a.i./kg soil (Visalia sandy loam), in the dark at 25 ± 0.1°C for 48 hours. 

The equilibrating solution used was 0.01M CaCl2 solution with a soil solution ratio of 

1.0:12.5 (w:v; 18 Acres sandy clay loam and Gartenacker loam); and 1.0:6.25 (w:v; Visalia 

sandy loam). The desorption phase of the study was carried out by replacing the adsorption 

solution with an equivalent volume of 0.01M CaCl2 solution and equilibrating in the dark at 

25 ± 0.1°C for 48 hours. A single desorption step was conducted for all soils. The 

experimental temperature employed during the study was reported to be maintained at 25 ±

0.1°C. The pH of the test solutions during the study ranged from 6.2-6.5. After 48 hours of 

equilibration, 58.0-68.3%, 46.3-59.5%, and 21.0-39.0% of the applied [14C]CGA380778 was 

adsorbed to the 18 Acres sandy clay loam, Gartenacker loam, and Visalia sandy loam soils, 

respectively. The Freundlich adsorption K values were 15.7, 10.3, and 1.7 for the 18 Acres 

sandy clay loam, Gartenacker loam, and Visalia sandy loam soils, respectively; 

corresponding Freundlich Koc values were 482, 501, and 361. The adsorption K and Koc

values were not determined. At the end of the desorption phase, the percent of 

[

14C]CGA380778 desorbed from the test soils, as percent of the radioactivity adsorbed, was 

93.0-174.2% for the 18 Acres sandy clay loam, 49.3-100.8% for the Gartenacker loam, and 

10.2-40.9% for the Visalia loam soils. The Freundlich desorption K values were 20.0, 13.5, 

and 3.8 for the 18 Acres sandy clay loam, Gartenacker loam, and Visalia sandy loam soils, 

respectively; corresponding Freundlich desorption Koc values were 615, 654, and 818. 

This study is classified as supplemental and upgradeable upon the submission of additional 

information related to classification of soils used in this study, in accordance to FAO Soil 

Classification (i.e. Soil Units) or equivalent U.S. Soil Taxonomy. The study was conducted 

using three soils. Additional study with a fourth soil is needed as required by the Subdivision 

N, Chemistry: Environmental Fate, Section 163-1 

164-1 Terrestrial Field Dissipation 

MRID 46800045 (Acceptable)

Soil dissipation/accumulation of mandipropamid (4-chloro-N-[2-[3-methoxy-4-(2-

propynyloxy)phenyl]ethyl]-α-(2-propynyloxy)benzeneacetamide) under U.S. field conditions 

was conducted in bare plots of sandy loam soil at one site in California. Mandipropamid was 

broadcast four times (7-day intervals) at a target rate of 0.165 kg a.i./ha (0.147 lb a.i./A) to a 
80

21 x 43 m test plot divided into three replicate areas. The total target rate applied was 660 g 

a.i./ha or 110% of the proposed maximum annual rate for leafy vegetables. The application 

was made to approximate the timing of typical fungicide applications in the fall for control of 

foliar oomycete pathogens on leafy vegetables in the San Joaquin Valley of California. Total 

water input during the study period was 70.32 inches or over 300% of the 30-year historical 

average precipitation. A control plot was located approximately 59 m from the treated plot. 

Soil samples were collected at 0, 1, and 6 days following the first three applications and at 0, 

1, 3, 7, 14, 21, 30, 58, 90, 125, 182, 272, 359, 454, and 540 days following the fourth 

application to a depth of 0-120 cm (except application 1, day-0 samples which were collected 

to a depth of 15 cm). 

The measured zero-time recovery of mandipropamid in the 0-15 cm soil layer was 56 ppb or 

70% of the theoretical. Mandipropamid was detected in the 0-15 cm soil layer at 97 ppb 

following the second application, 146 ppb following the third application, and at a maximum 

of 165 ppb following the fourth application. Following the fourth application, 

mandipropamid decreased to 83 ppb by 58 days, 31 ppb by 182 days, 4.1 ppb by 272 days, 

and ranged from 2.1-2.6 ppb from 359 to 540 days posttreatment. Mandipropamid was not 

detected below the 0-15 cm soil depth. No transformation products were detected in the soil 

at greater than 10% of the applied mandipropamid. Under field conditions at the test site, 

mandipropamid had a half-life value of 75.3 days in soil (r2

 = 0.9158), calculated using linear 

regression and the equation t1⁄2 = ln 2 / k, where k is the rate constant, and based on all 

available data following the fourth application. The major route of dissipation of 

mandipropamid under terrestrial field conditions could not be determined because 

transformation products were detected at <2% of the applied mandipropamid, leaching and 

carryover of residues were not observed, and volatilization and runoff were not studied. 

However, the study author stated that no major degradation product was identified in the 

laboratory environmental fate studies. 

MRID 46800046 (Acceptable)

Soil dissipation/accumulation of mandipropamid (4-chloro-N-[2-[3-methoxy-4-(2-

propynyloxy)phenyl]ethyl]-α-(2-propynyloxy)benzeneacetamide) under U.S. field conditions 

was conducted in a bare plot and a cropped plot (potatoes) of loamy sand soil at one site in 

New York. Mandipropamid was broadcast four times (6- to 7-day intervals) at a target rate of 

0.165 kg a.i./ha (0.147 lb a.i./A) to two 29 x 35 m test plots each divided into three replicate 

areas. The total target rate applied was 660 g a.i./ha or 110% of the proposed maximum 

annual rate for potatoes. The potato crop was at the late bloom stage (20-inch height) at the 

first application and at the post bloom stage (24-inch height) at subsequent applications; 

coverage was 70% at the first application and 85-90% by the fourth application. The crop 

was harvested 57 days after the fourth application. The application was made to approximate 

the timing of typical fungicide applications for control of oomycete pathogens (late blight) on 

potatoes in the Northeastern region of the U.S. Total water input during the study period was 
81

80.60 inches or 142% of the 30-year historical average precipitation. A control plot was 

located approximately 70 m from the nearest treated plot. Soil samples were collected at 0, 1, 

and 5 days following the first application, at 0, 1, and 6 days following the second and third 

applications, and at 0, 1, 3, 7, 14, 21, 30, 65, 91, 124, 194, 275, 356, 448, and 505 days 

following the fourth application to a depth of 0-120 cm (except application 1, day-0 samples 

which were collected to a depth of 15 cm). 

In the bare plot, the measured zero-time recovery of mandipropamid in the 0-15 cm soil layer 

was 68 ppb or 79% of the theoretical. Mandipropamid was detected in the 0-15 cm soil layer 

at 100 ppb following the second application, 136 ppb following the third application, and 120 

ppb following the fourth application. Following the fourth application, mandipropamid 

decreased to 63-65 ppb by 7-21 days, 43-54 ppb by 30-194 days, 12 ppb by 275 days, and 

ranged from 2.7-4.4 ppb from 356 to 505 days posttreatment. Mandipropamid was not 

detected below the 0-15 cm soil depth. No transformation products were detected in the soil 

at greater than 10% of the applied mandipropamid. In the cropped plot, the measured zerotime recovery of mandipropamid in the 0-15 cm soil layer was 52 ppb or 60% of the 

theoretical. Mandipropamid was detected in the 0-15 cm soil layer at 53 ppb following the 

second application, 90 ppb following the third application, and 101 ppb following the fourth 

application. Following the fourth application, mandipropamid increased to a maximum of 

167 ppb by 65 days, coinciding with the sampling interval following the harvest of the potato 

crop at 57 days posttreatment, when residues bound to the potato leaves were incorporated 

into the soil. Following 65 days, mandipropamid decreased to 68 ppb by 194 days, 20-21 ppb 

by 356-448 days, and was 16 ppb at 505 days posttreatment. Mandipropamid was not 

detected below the 0-15 cm soil depth. No transformation products were detected in the soil 

at greater than 10% of the applied mandipropamid. Under field conditions in the bare plot, 

mandipropamid had a half-life value of 100.5 days in soil (r2 = 0.8628), calculated using 

linear regression and the equation t1⁄2 = ln 2 / k, where k is the rate constant, and based on all 

available data following the fourth application. However, dissipation was bi-phasic, with a 

more rapid decline phase during the first month of the study; the half-life based on 0-30 day 

data was 27.8 days (r2

 = 0.5521). 

Under field conditions in the cropped plot, mandipropamid had a half-life value of 126 days 

in soil (r2

 = 0.9384), calculated using linear regression and the equation t1⁄2 = ln 2 / k, where k 

is the rate constant, and based on all available data following the maximum detection of 

mandipropamid at 65 days following the fourth application. The major route of dissipation of 

mandipropamid under terrestrial field conditions could not be determined because 

transformation products were detected at <2% of the applied mandipropamid, leaching and 

carryover of residues were not observed (carryover was <5%), and volatilization and runoff 

were not studied. However, the study author stated that there was no major degradation 

product identified in the laboratory environmental fate studies. 

MRID 46800047 (Acceptable)

Soil dissipation/accumulation of mandipropamid (4-chloro-N-[2-[3-methoxy-4-(2-

propynyloxy)phenyl]ethyl]-α-(2-propynyloxy)benzeneacetamide) under US field conditions 
82

was conducted in bare plots of loamy sand soil at one site in Georgia. Mandipropamid was 

broadcast four times (7-day intervals) at a target rate of 0.165 kg a.i./ha (0.147 lb a.i./A) to a 

35 x 35 m test plot divided into three replicate areas. The total target rate applied was 660 g 

a.i./ha or 110% of the proposed maximum annual rate for squash. The applications were 

made to approximate the timing of typical fungicide applications in the spring for control of 

oomycete pathogens on squash in the Southeastern region of the U.S. Total water input 

during the study period was 138.54 inches or 189% of the 30-year historical average 

precipitation. A control plot was located approximately 46 m from the treated plot. Soil 

samples were collected at 0, 1, and 6 days following the first three applications and at 0, 1, 3, 

7, 14, 21, 30, 62, 93, 120, 183, 268, 364, 457, and 540 days following the fourth application 

to a depth of 0-120 cm (except application 1, day-0 samples which were collected to a depth 

of 15 cm). The measured zero-time recovery of mandipropamid in the 0-15 cm soil layer was 

58 ppb or 76% of the theoretical. Mandipropamid was detected in the 0-15 cm soil layer at 86 

ppb following the second application, a maximum of 136 ppb following the third application, 

and 124 ppb following the fourth application. Following the fourth application, 

mandipropamid decreased to 60 ppb by 21 days, 19 ppb by 62 days, 4.0-5.9 ppb by 268-364 

days, and was 0.74 ppb at 540 days posttreatment. Mandipropamid was only detected in the 

15-30 cm soil depth once, at 0.53 ppb at 14 days posttreatment, and was not detected below 

that depth. No transformation products were detected in the soil at greater than 10% of the 

applied mandipropamid. Under field conditions at the test site, mandipropamid had a half-life 

value of 81.5 days in soil (r2

 = 0.8934), calculated using linear regression and the equation t1⁄2

= ln 2 / k, where k is the rate constant, and based on all available data following the fourth 

application. However, dissipation was bi-phasic, with a more rapid decline phase during the 

first two months of the study; the half-life based on 0-62 day data was 24.5 days (r2 = 

0.9090). The major route of dissipation of mandipropamid under terrestrial field conditions 

could not be determined because transformation products were detected at <2% of the 

applied mandipropamid, leaching and carryover of residues were not observed, and 

volatilization and runoff were not studied. However, the study author stated that there was no 

major degradation product identified in the laboratory environmental fate studies. 

The important metabolites formed by the degradation of mandipropamid are provided in 

Table A-7 and the chemical structures of these metabolites are illustrated in Table A-8. 
83

Table A-7. Maximum Amounts of Mandipropamid Metabolites in Degradation Studies 

Characterized by Study Type 

Study Type Metabolite (% Maximum) MRID 

161-1 Hydrolysis No degradation products observed 46800007,8 

161-2 Aqueous photolysis Polar compounds totaled average 

of 36.7%. 

Unidentified polar compounds 

totaled a maximum of 25.0%. 

Unidentified minor residues 

maximum of ≤6.2% of the applied 

minor nonpolar transformation 

products, none averaging >5% of 

the applied 

46800009 

46800010 

46800011,12 

46800013,14 

161-3 Soil photolysis CO2 (6.3%) 

CGA380775 (4.1%) 

SYN505503 (3.0%) 

CGA380778 (2.5%) 

NOA495119 (0.2%) 

NOA458422 (0.7%) 

SYN521195 (not quantified) 

CO2 (17.1%) 

CGA380778 (3.9%) 

CO2 (`14.98%) 

CGA380778 (3.80%) 

46800015 

46800016,17 

46800018,19 

162-1 Aerobic soil metabolism CO2 (maximum 56.3% 

CGA380778 (4.25%) 

CGA380775 (0.51%) 

SYN500003 (0.27%) 

NOA458422 (0.18%) 

CGA380778 (2.9%) 

CO2 (maximum 51.0%) 

CO2 (21.8%) 

CGA380778 (1.4%) 

SYN536638 (2.4%) 

NOA458422 (below limit of 

detection 

CGA380778 (3.2%) 

CO2 (12.3%) 

CGA380778 (4.8%) 

46800020,21 

46800022 

46800023 

46800024,25 

46800027 

46800028 
84

Table A-7. Maximum Amounts of Mandipropamid Metabolites in Degradation Studies 

Characterized by Study Type 

Study Type Metabolite (% Maximum) MRID 

162-2 Anaerobic soil metabolism CO2 was the only significant 

degradation product. 

CGA380778(4.6%) 

46800022 

162-3 Anaerobic aquatic 

metabolism 

SYN500003 (25.9%) 

YN504851 (73.5%) 

YN521195 (10.3%) 

O2 (15.8%) 

YN539678 (4.6%) 

YN539679 (6.1%) 

SYN536638 (0.9%)

46800030,31 

162-4 Aerobic aquatic metabolism SYN521195 (10.8%) 

SYN504851 (11.1%) 

SYN500003 (6.4%) 

SYN539678 (6.9%) 

SYN539679 (0.9%) 

SYN536638 (1.9) 

46800032 
85

Table A-8. The Chemical Structure of NOA446510 (Mandipropamid) and its 

Metabolites 

CH

C

2CH

O

C

H2

Cl

N O CH3

O

C

H2

C

H O 2

C

CH

NOA446510

Cl

O

N

O

C

H2

C

H2

OH

OH

CH2

C

CH

SYN505503

Cl

OH

O

N

C

H2

C

H2

O

O CH3

C

H2

C

CH

CGA380778 

Cl

O

N

OH

C

H2

C

H2

OH

O

CH3

CGA380775 
86

Table A-8. The Chemical Structure of NOA446510 (Mandipropamid) and its 

Metabolites 

Cl

O

O

N

2CH

C

CH

C

H2

C

H2

O

O

C

H2

C

CH3

SYN536638 

Cl

O

O

N

2CH

C

CH

C

H2

C

H2

O

OH

C

H2

C

CH

SYN521195 

Cl

O

O

N

2CH

C

CH

C

H2

C

H2

O

OH

C

H2

C

SYN539678 
87

Table A-8. The Chemical Structure of NOA446510 (Mandipropamid) and its 

Metabolites 

Cl

O

O

OH

2CH

C

SYN504851

Cl

O

O

N

2CH

C

C

H2

C

H2

O

OH

C

H2

C

SYN539679 
88

Appendix B. GENEEC Aquatic Exposure Model 

The GENEEC (GENeric Estimated Environmental Concentration) model, the tier one 

computer program, uses the soil/water partition coefficient and degradation kinetic data to 

estimate runoff from a ten hectare field into a one hectare by two meter deep "standard" 

pond. This first tier is designed as a coarse screen and estimates conservative pesticide 

concentrations in surface water from a few basic chemical parameters and pesticide label use 

and application information. Tier 1 is used to screen chemicals to determine which ones 

potentially pose sufficient risk to warrant higher level modeling. Chemicals failing to pass 

this program, move on to the tier two modeling. As a matter of policy, OPP does not take 

significant adverse regulatory action based upon the results of tier 1 screening models. 

GENEEC is a program to calculate acute as well as longer-term estimated environmental 

concentration (EEC) values. It considers reduction in dissolved pesticide concentration due to 

adsorption of pesticide to soil or sediment, incorporation, degradation in soil before washoff 

to a water body, direct deposition of spray drift into the water body, and degradation of the 

pesticide within the water body 

((http://www.epa.gov/oppefed1/models/water/geneec2_users_manual.htm#introduction)). 

GENEEC Output 

RUN No. 1 FOR Total Residue ON all * INPUT VALUES * 

-------------------------------------------------------------------- 

RATE (#/AC) No.APPS & SOIL SOLUBIL APPL TYPE NO-SPRAY INCORP 

ONE(MULT) INTERVAL Koc (PPM ) (%DRIFT) ZONE(FT) (IN) 

-------------------------------------------------------------------- 

.130( .477) 4 7 2.9******* AERL_B( 13.0) .0 .0 

FIELD AND STANDARD POND HALFLIFE VALUES (DAYS) 

-------------------------------------------------------------------- 

METABOLIC DAYS UNTIL HYDROLYSIS PHOTOLYSIS METABOLIC COMBINED 

(FIELD) RAIN/RUNOFF (POND) (POND-EFF) (POND) (POND) 

-------------------------------------------------------------------- 

72.04 2 N/A 1.10- 136.40 102.00 58.36 

GENERIC EECs (IN MICROGRAMS/LITER (PPB)) Version 2.0 Aug 1, 2001 

-------------------------------------------------------------------- 

PEAK MAX 4 DAY MAX 21 DAY MAX 60 DAY MAX 90 DAY 

GEEC AVG GEEC AVG GEEC AVG GEEC AVG GEEC 

-------------------------------------------------------------------- 

20.88 20.67 19.42 16.92 15.29 
89

APPENDIX C. Explanation of T-REX Model 

1. Introduction 

This spreadsheet based model calculates the decay of a chemical applied to foliar surfaces for 

single or multiple applications. It uses the same principle as the batch code models FATE and 

TERREEC for calculating terrestrial estimates exposure (TEEC) concentrations on plant 

surfaces following application. A first-order decay assumption is used to determine the 

concentration at each day after initial application based on the concentration resulting from 

the initial and additional applications. The decay is calculated by from the first-order rate 

equation: 

CT = Cie

-kT

or in log form: 

ln (CT/Ci) = kT 

where: 

CT = concentration at time T = day zero. 

Ci = concentration, in parts per million (ppm) present initially (on day zero) on the 

surfaces. Ci is calculated based on Kenaga and Fletcher by multiplying the Ci

based on the Kenaga nomogram (Hoerger and Kenaga [1972] as modified by 

Fletcher [1994]). For maximum concentration the application rate, in pounds 

active ingredient per acre, is multiplied by 240 for short grass, 110 for tall 

grass, and 135 for broad leafed plants/small insects and 15 for 

fruits/pods/large insects. Additional applications are converted from pounds 

active ingredient per acre to ppm on the plant surface and the additional mass 

added to the mass of the chemical still present on the surfaces on the day of 

application. 

k = If the foliar dissipation data submitted to EFED are found scientifically valid 

and statistically robust for a specific pesticide, the 90% upper-confidence limit 

of the mean half-lives should be used. When scientifically valid, statistically 

robust data are not available TETT recommends the use of a default half-life 

value of 35 days. The use of the 35 day half-life is based on the highest 

reported value (36.9 days) reported by Willis and McDowell (1987). 

T = time, in days, since the start of the simulation. The initial application is on day 

0. The simulation is designed to run for 365 days. 
90

The program calculates concentration on each type of surface on a daily interval for one year. 

The maximum concentrations during the year are calculated for both maximum and mean 

residues. The inputs required are: 

Application rate: The maximum label application rate (in pounds 

a.i./acre)

Half-life: The degradation half-life for the dominate 

process (in days)

Frequency of application: The interval between repeated applications, from 

the label (in days)

Maximum number of application per year: From the label

The calculated concentrations are used to calculate Avian and Mammalian RQ values. The 

maximum calculated concentration is divided by user input values for acute and chronic 

endpoints to give RQs for each type of plant surface. 

2. Avian Species 

For calculating dose-based RQs in birds, the maximum and mean Kenaga residue values are 

adjusted for avian class and food consumption based on the following scaling factor (USEPA 

1993): 

FI (g/d) = 0.648 (g bw)^0.651 

For the three avian weight classes considered (20, 100, and 1000 g), this results in percent of 

body weight consumption of: 

Weight (g) FI Wet FI

% Body 

Weight 

Consumed

20 4.555599463 22.77799731 114 

100 12.98897874 64.94489369 65 

1000 58.15338588 290.7669294 29 

A. Dose-Based Acute RQs 

Dose-based acute RQs are then calculated using the formula: 

RQ = adjusted EEC/LD50 or NOAEL 

where the adjusted EEC is considered to be the daily dose weighted for percent of body 

weight consumed of a given food source. 
91

B. Dietary-Based RQs 

For dietary-based RQs, two values are given for each food group. First, the consumptionweighted RQ for each weight class (20, 100, and 1000 g birds) is displayed and calculated 

using the equation: 

RQ = EEC/((LC50 or NOAEC)/(%bw consumed)) 

In the second method, no adjustment is made for consumption differences among the weight 

classes. This RQ is calculated: 

RQ = EEC/LC50 or NOAEC 

3. Mammalian Species 

A. Dose-Based RQs 

For calculating dose-based RQs in mammals, the maximum and mean Kenaga values are 

adjusted for mammalian class and food consumption (0.95, 0.66, and 0.15 body weight for 

herbivores and insectivores and 0.21, 0.15, and 0.03 body weight for granivores). Dose-based 

acute and chronic RQs are then calculated by dividing the adjusted EECs (daily dose) by the 

LD50 or NOAEL. 

B. Dietary-Based RQs 

Dietary-based RQs are calculated using the equation: 

RQ = EEC/((LC50 or NOAEC)/(% bw consumed)) 

4. Graph 

A graph of concentration on each plant surface vs. time is plotted and a concentration of 

concern line can be added at a user specified level. The concentration of concern (e.g., avian 

LC50, mammalian NOAEL) label should be entered in the cell underneath the value. The 

graph automatically plots a line at this concentration and the label is extracted from that cell. 

The graph is plotted for the first 100 days post-application. Graphs displaying acute and 

chronic LOCs for both birds and mammals are displayed in the "Graph" worksheet. These 

graphs may be useful as a visual aid to communicate risk in your assessment and can be 

copy/pasted into your document. To help with scaling issues on the y axis, you may want to 

delete one of the endpoints. 

5. New Version Notes 

A new look is used in this update in an effort to decrease confusion and increase transparency 

in the risk assessment process. This version of T-REX (v1.3.1) incorporates the ability to 

calculate EECs and RQs for maximum and mean residues. Mean residues are calculated 
92

exactly as the maximum residues are, except the corresponding Kenaga values are: 85 for 

short grass, 36 for tall grass, and 45 for broad leafed plants/small insects and 7 for 

fruits/pods/large insects. 
93

Appendix D. Explanation of TerrPlant Model

Introduction 

Exposure to Terrestrial Plants including Wetlands (December 26, 2005; version 1.2.1) 

The change to this model version is the removal of the 60% efficiency factor for aerial 

applications. 

Terrestrial plants inhabiting dry and semi-aquatic (wetland) areas may be exposed to 

pesticides from runoff and/or spray drift. Semi-aquatic areas are low-lying wet areas that may 

dry up at times throughout the year. 

EFED's runoff scenario is: 

(1) based on a pesticide's water solubility and the amount of pesticide present on the soil 

surface and its top one centimeter; 

(2) characterized as "sheet runoff" (one treated acre to an adjacent acre) for dry areas; 

(3) characterized as "channel runoff" (10 acres to a distant low-lying acre) for semiaquatic or wetland areas; and 

(4) based on percent runoff values of 0.01, 0.02, and 0.05 for water solubilities of <10, 

10–100, and <100 ppm, respectively. 

EFED's Spray Drift scenario is assumed as: (1) 1% for ground application; and (2) 5% for 

aerial, airblast, forced air, and spray chemigation applications. 

The spray drift ratio used here is in agreement with the policy procedures at the time the 

worksheet was designed. 

Currently, (1) this worksheet is designed to derive the plant exposure concentrations from a 

single, maximum application rate only; and (2) for pesticide applications with incorporation 

of depth of less than 1 inch, the total loading EECs derived for the incorporation method will 

be same as the unincorporated method. 

To calculate RQ values for Non-Endangered Terrestrial Plants: 

Terrestrial Plants Inhabiting Areas Adjacent to Treatment Site: 

Emergence RQ = Total Loading to Adjacent Area or EEC/Seedling Emergence EC25

Drift RQ = Drift EEC/Vegetative Vigor EC25
94

Terrestrial Plants Inhabiting Semi-aquatic Areas Adjacent to Treatment Site: 

Emergence RQ = Total Loading to Semi-aquatic Area or EEC/Seedling Emergence EC25

Drift RQ = Drift EEC/Vegetative Vigor EC25

To calculate RQ values for Endangered Terrestrial Plants: 

Endangered Terrestrial Plants Inhabiting Areas Adjacent to Treatment Site: 

Emergence RQ = Total Loading to Adjacent Area or EEC/Seedling Emergence EC05 or 

NOAEC 

Drift RQ = Drift EEC/Vegetative Vigor EC05 or NOAEC 

Endangered Terrestrial Plants Inhabiting Semi-aquatic Areas Near Treatment Site: 

Emergence RQ = Total Loading to Semi-aquatic Area or EEC/Seedling Emergence EC05 

or NOAEC 

Drift RQ = Drift EEC/Vegetative Vigor EC05 or NOAEC 

Background for EEC Calculation 

Formulas used to calculate EEC values (November 9, 2005; version 1.2.1) 

To calculate EECs for terrestrial plants inhabiting in areas adjacent to treatment sites: 

Un-incorporated Ground Application (Non-granular):

Sheet Runoff = Application Rate (lbs a.i./acre) x Runoff Value 

Drift = Application Rate (lbs a.i./acre) x 0.01 

Total Loading = EEC = Sheet Runoff + Drift 

Incorporated Ground Application with Drift (Non-granular): 

Sheet Runoff = [Application Rate (lbs a.i./acre)/Incorporation Depth (cm)] x Runoff 

Value 

Drift = Application Rate (lbs a.i./acre) x 0.01 

Total Loading = EEC = Sheet Runoff + Drift 

Un-incorporated Ground Application (Granular): 

Sheet Runoff = EEC = Application Rate (lbs a.i./acre) x Runoff Value 

Incorporated Ground Application without Drift (Granular): 

Sheet Runoff = EEC = [Application Rate (lbs a.i./acre)/Incorporation Depth (cm)] x 

Runoff Value 
95

Aerial/Airblast/Spray Chemigation Applications1

: 

Sheet Runoff = Application Rate (lbs a.i./acre) x Runoff Value 

Drift = Application Rate (lbs a.i./acre) x 0.05 

Total Loading = EEC = Sheet Runoff + Drift 

Runoff Value = 0.01, 0.02, or 0.05 when the solubility of the chemical is <10 ppm, 10-100 

ppm, or >100 ppm, respectively. Incorporation Depth: Use the minimum incorporation depth 

reported on the label. 

Formulas used to calculate EEC values: 

To calculate EECs for terrestrial plants inhabiting semi-aquatic low-lying areas near 

treatment sites: 

Un-incorporated Ground Application (Non-granular):

Channelized Runoff = Application Rate (lbs a.i./acre) x Runoff Value x Factor 10 

Drift = Application Rate (lbs a.i./acre) x 0.01 

Total Loading = EEC = Channelized Runoff + Drift 

Incorporated Ground Application with Drift (Non-granular): 

Channelized Runoff = [Application Rate (lbs a.i./acre)/Incorporation Depth (inch)] x 

Runoff Value x Factor 10 

Drift = Application Rate (lbs a.i./acre) x 0.01 

Total Loading = EEC = Channelized Runoff + Drift 

Un-incorporated Ground Application (Granular): 

Channelized Runoff = EEC = Application Rate (lbs a.i./acre) x Runoff Value x Factor 10 

Incorporated Ground Application without Drift (Granular): 

Channelized Runoff = EEC = [Application Rate (lbs a.i./acre)/Incorporation Depth 

(inch)] x Runoff Value x Factor 10 

Aerial/Airblast/Spray Chemigation Applications: 

Channelized Runoff = Application Rate (lbs a.i./acre) x Runoff Value x Factor 10 

Drift = Application Rate (lbs a.i./acre) x 0.05 

Total Loading = EEC = Channelized Runoff + Drift 
96

Runoff Value = 0.01, 0.02, or 0.05 when the solubility of the chemical is <10 ppm, 10-100 

ppm, or >100 ppm, respectively. Factor 10 represents 10 treated acres per acre of low-lying 

area. Incorporation Depth: Use the minimum incorporation depth reported on the label.
97

Appendix E. Description of Ecological Effects 

Studies 

a. Toxicity to Terrestrial Animals 

I. Birds, Acute and Subacute

An acute oral toxicity study using the technical grade of the active ingredient (TGAI) is 

required to establish the toxicity of mandipropamid to birds. The preferred test species is 

either mallard duck (a waterfowl) or bobwhite quail (an upland gamebird). Results of this 

test are tabulated below. 

Avian Acute Oral Toxicity 

Species % a.i. LD50 

(mg/kg 

a.i.) 

Toxicity Category 

MRID No. Study 

Classification1

Mallard Duck 

(Anas platyrhychos)

96.5 > 1000 Practically 

nontoxic 

468001-11 Acceptable 

Northern Bobwhite Quail 

(Colinus virginianus) 

96.5 

> 2250 Practically 

nontoxic 

468001-10 Acceptable 

The results of these studies demonstrate that mandipropamid is practically nontoxic to avian 

species on an acute oral basis. 

Two subacute dietary studies using the TGAI are required to establish the toxicity of 

mandipropamid to birds. The preferred test species are mallard duck and bobwhite quail. 

Results of these tests are tabulated below. 

Avian Subacute Dietary Toxicity 

Species % a.i. 

5-Day 

LC50 

(ppm a.i.) 

Toxicity Category 

MRID No. 

Study 

Classification1

Mallard Duck 

(Anas platyrhychos) 

96.5 > 6080 Practically 

Nontoxic 

468001-12 Acceptable 

Northern Bobwhite 

Quail 

(Colinus 

virginianus)

96.5 

> 6080 Practically 

Nontoxic 

468001-13 Acceptable 
98

The results of the avian acute dietary studies indicate mandipropamid is practically nontoxic 

to avian species on a subacute dietary basis. 

ii. Birds, Reproductive Toxicity

Two avian reproduction studies testing mandipropamid were submitted to the Agency. The 

details of these studies are illustrated in the following table. The results of these studies 

demonstrated no significant effects to either avian reproduction or growth. 

Avian Reproductive Toxicity 

Species/ 

Exposure 

Duration 

% a.i. 

Test 

Type 

Toxicity 

Value (ppm) 

Affected 

Endpoints 

MRID 

No. 

Study 

Classification 

Mallard Duck 

(Anas 

platyrhychos) 

96.5 Avian 

Reproduction 

NOAEC: 1060 

LOAEC: > 1060 

None 467152-

14 

Acceptable 

Northern 

Bobwhite 

(Colinus 

virginianus) 

96.5 Avian 

Reproduction 

NOAEC: 1060 

LOAEC: > 1060 

None 468001-

15 

Acceptable 

iii. Mammals, Acute and Chronic 

Wild mammal testing is required on a case-by-case basis, depending on the results of lower 

tier laboratory mammalian studies, intended use pattern and pertinent environmental fate 

characteristics. In most cases, rat or mouse toxicity values obtained from the Agency's 

Health Effects Division (HED) substitute for wild mammal testing. A rat multigenerational 

study and a rat acute oral toxicity study have been submitted to the Agency. The toxicity 

values for this study are tabulated below. 

Mammalian Toxicity 

Species 

% a.i. 

Test 

Type 

Toxicity 

Value 

Affected 

Endpoints 

MRID 

No. 

Study 

Classification 

Laboratory 

Rat 

(Rattus 

norvegicus) 

Technical Rat Multigenerational 

Reproduction 

toxicity 

250 ppm Decreased body 

weights, weight 

gains, food 

consumption, 

and food 

utilization 

468002

-30 

Acceptable 

Laboratory 

Rat 

(Rattus norvegicus) 

Technical Rat Acute 

Oral Toxicity 

> 5000 

mg/kg 

No mortality MRID 

468002

-30 

Acceptable 
99

iv. Terrestrial Invertebrates 

A honey bee acute contact study using the TGAI is required for mandipropamid because its 

proposed uses may result in honey bee exposure. Results of this test are tabulated below. 

Non-target Insect Acute Contact Toxicity 

Species % 

a.i. 

LD50 

(ug/bee) Toxicity 

Category 

MRID No. Study 

Classification 

Honey Bee 

(Apis mellifera L.) 

99 % > 200 ug 

ai/bee 

Practically nontoxic 

468001-16 Acceptable 

The registrant has also submitted two earthworm acute toxicity studies. One of the studies 

tested the TGAI and the other study tested the mandipropamid degradate, CGA380778. The 

results of these studies are illustrated in the table below. 

Earthworm Acute Toxicity Test Toxicity 

Species 

Chemical 

% 

purity LC50

Toxicity 

Category 

MRID 

No. 

Study 

Classification 

Earthworms 

(Eisenia 

fetida) 

Mandipropamid 99 >1000 

mg ai/kg 

dw of 

soil. 

Nontoxic at 

the highest 

concentration

s tested 

468001-

23 

Acceptable 

Earthworms 

(Eisenia 

fetida) 

CGA380778 

(Mandipropamid 

Degradate) 

99 >1000 

mg ai/kg 

dw of 

soil. 

Nontoxic at 

the highest 

concentration

s tested 

468001-

22 

Acceptable 

The above analysis of the results show that mandipropamid is practically non-toxic to honey 

bees and that mandipropamid and its’ degradate, CGA380778, is nontoxic to earthworms at 

the highest concentrations tested. Therefore, it is presumed that the use of mandipropamid 

will not pose a significant risk to non-target terrestrial invertebrates. 
100

b. Toxicity to Freshwater Aquatic Animals

I. Freshwater Fish, Acute

Two freshwater fish acute toxicity studies using the TGAI are required to establish the 

toxicity of mandipropamid to fish. The preferred test species are rainbow trout (a coldwater 

fish) and bluegill sunfish (a warmwater fish). The registrant has submitted 3 freshwater fish 

acute toxicity studies. Two of the studies tested the TGAI and one tested, CGA380778. 

Currently, all of the registrant submitted freshwater fish toxicity studies testing 

mandipropamid and the mandipropamid degradate, CGA380778, are deemed invalid. The 

studies were invalidated because of the failure of the study authors to take appropriate 

measures to ensure the test chemical was adequately dissolved in the test water. This was 

indicated by the failure of the measured concentrations to remain at least 80% of the nominal 

concentrations, as required by the fish acute toxicity Guideline, 850.1075. Additionally, the 

test solutions contained undissolved particulate test material. This was an additional 

indication of the failure to successfully dissolve the test solution. Solubility is defined by the 

Agency’s Pesticide Registration Rejection Rate Analysis Document as the amount of 

chemical retained in the supernatant of a conventionally centrifuged sample of test media. 

Because the test material was not adequately dissolved, it was not possible to obtain accurate 

toxicity endpoint values that could be used for risk assessment purposes. Further details 

regarding these studies are listed in the table below. 
101

Freshwater Fish Acute Toxicity 

Species 

Chemical 

% purity 

96-

hour 

LC50 

(a.i. 

ppm) 

NOAEC 

(ppm 

a.i.) Toxicity 

Category 

MRID 

No. 

Author/

Year 

Study 

Classification 

Fathead 

Minnow 

(Pimephales 

promelas) 

Mandipropamid 

96.1% a.i. 

> 5.8 4.4 Note 1 Undeterminable

Note 4

468001-

05 

Invalid Note 5

Rainbow trout 

(Oncorhynchu

s mykiss)

Mandipropamid 

96.1% a.i. 

4.4 1.7 Note 2 Undeterminable 

Note 4

468001-

06 

Invalid Note 5

Rainbow trout 

(Oncorhynchu

s mykiss)

CGA380778 > 43 9.3 Note 3 Undeterminable 

Note 4

468001-

04 

Invalid Note 5

Note 1: The NOAEC value, based on sub-lethal effects, was 4.4 mg a.i./L. Sub-lethal effects (loss of 

equilibrium and lethargy) were observed in the group exposed to 5.8 mg a.i./L of NOA446510 

(Mandipropamid). As no sub-lethal quantitative measurements were taken, the reviewer was unable to 

determine an EC50 value. 

Note 2: This NOAEC value based on mortality and sub-lethal effects, was 1.7 mg a.i./L. Sub-lethal effects 

(surfacing, lying on the bottom of the aquarium, loss of equilibrium, lethargy, erratic swimming and 

morphological deformity) were observed in the groups exposed to mean-measured concentrations 3.1-6.5 

mg a.i./L of NOA446510. As no sub-lethal quantitative measurements were taken, the reviewer was unable 

to determine an EC50 value. 

Note 3: This NOAEC is value, based on mortality and sub-lethal effects, was 9.3 mg/L. Sub-lethal effects 

(quiescence, sounding, dark discoloration, loss of balance, ceased swimming, labored respiration and 

swollen abdomen) were observed in the groups exposed to 17-43 mg/L of CGA380778. As no sub-lethal 

quantitative measurements were taken, the reviewer was unable to determine an EC50 value. 

Note 4: Because of the failure of the mean measured concentrations to remain at least 80% of the nominal 

concentrations, the concentrations in which these effects were observed cannot be validated. 

Note 5: The studies were invalidated because of the failure of the study authors to take appropriate 

measures to ensure the test chemical was adequately dissolved in the test water. This was indicated by the 

failure of the measured concentrations to remain at least 80% of the nominal concentrations, as required by 

the fish acute toxicity Guideline, 850.1075.

ii. Fish, Chronic toxicity. 

Mandipropamid is mobile and is likely to readily and frequently (due to multiple applications 

during a growing season) reach surface water bodies. Thus, a fish chronic toxicity study 

testing mandipropamid is required. The registrant has submitted a fish early life-stage 
102

chronic toxicity study testing the TGAI. The results of the study demonstrated a NOAEC of 

0.210 ppm based on growth. The details of this study are listed in the table below. 

Freshwater Fish Chronic Toxicity 

Species % ai 

Chronic 

Toxicity 

NOAEC and 

LOAEC 

(a.i. ppm) 

Most sensitive 

Endpoint 

Affected MRID No. 

Author/Year 

Study 

Classification 

Fathead 

minnow 

96.5 NOAEC: 0.22 

LOAEC: 

0.47 

Length, wet and 

dry weight 

468001-08 Acceptable 

iii. Freshwater Invertebrates, Acute

A freshwater aquatic invertebrate toxicity test using the TGAI is required to establish the 

toxicity of mandipropamid to aquatic invertebrates. The preferred test species is Daphnia 

magna. Results of this test are tabulated below. The registrant has submitted a study testing 

the TGAI and a study testing the mandipropamid degradate, CGA380778. 

Freshwater Invertebrate Acute Toxicity for Mandipropamid and a Mandipropamid 

degradate, CGA380778 

Species 

Chemical (% 

purity). 

48-hour 

EC50 

(ppm 

a.i.) 

NOAEC 

(ppm a.i.; 

based on 

mortality) Toxicity 

Category 

MRID 

No. 

Study 

Classification 

Waterflea 

(Daphnia 

magna) 

Mandipropamid 

(96.5 %) 

7.1 4.7 Moderately 

toxic 

468001-

50 

Acceptable 

Waterflea 

(Daphnia 

magna) 

CGA380778 

(98%) 

54.2 37 Slightly 

Toxic 

468001-

51 

Acceptable 

Since the EC50 for the TGAI, mandipropamid, falls in the range of 1 - 10 ppm, 

mandipropamid is moderately toxic to aquatic invertebrates on an acute basis. Since the 

EC50 for the major degradate of mandipropamid, CGA380778 falls in the range of 10 ppm – 

100 ppm, CGA380778 is classified as practically nontoxic to freshwater invertebrates. 
103

iv. Freshwater Invertebrate, Chronic 

Mandipropamid is highly mobile and is likely to readily and frequently (due to multiple 

applications during a growing season) reach surface water bodies. Thus, invertebrate chronic 

toxicity testing mandipropamid is required. The registrant has submitted one freshwater 

invertebrate chronic toxicity study however the study was deemed invalid. The study was 

invalid because reproduction of solvent control daphnids was significantly lower than that of 

negative control daphnids. According to the EPA memo titled, “Interim Policy Guidance for 

the Use of Dilution-Water (Negative) and Solvent Controls in Statistical Data Analysis for 

Guideline Aquatic Toxicology Studies”, dated March 30, 2006, the study exhibiting such 

results would be invalidated. The details of the study are demonstrated below. 

Freshwater Invertebrate Chronic Toxicity 

Species 

% ai 

Chronic 

Toxicity 

NOAEC and 

LOAEC 

(a.i. ppm) 

Most sensitive 

Endpoint 

Affected 

MRID No. 

Author/Year 

Study 

Classification 

Daphnia 

magna 

99 * NOAEC: 

< 0.023 

LOAEC: 

0.023 

Reproduction 468001-07 Invalid Note 1

* Note: The reviewer’s analysis showed that reproduction of solvent control daphnids was significantly lower 

than that of negative control daphnids, which according to the EPA memo titled, “Interim Policy Guidance for 

the Use of Dilution-Water (Negative) and Solvent Controls in Statistical Data Analysis for Guideline Aquatic 

Toxicology Studies”, dated March 30, 2006, would result in the INVALID classification of this study. 

c. Toxicity to Estuarine/Marine Animals

I. Estuarine/Marine Fish, Acute

Mandipropamid usage may occur in some areas associated with marine/estuarine habitats. Thus, 

marine/estuarine fish toxicity data is required. There are two registrant submitted acute toxicity 

studies testing marine/estuarine fish. However both studies were deemed invalid. The studies 

were invalidated because of the failure of the study authors to take appropriate measures to 

ensure the test chemical was adequately dissolved in the test water. This was indicated by the 

failure of the measured concentrations to remain at least 80% of the nominal concentrations, as 

required by the fish acute toxicity Guideline, 850.1075. Additionally, the test solutions 

contained undissolved particulate test material. This was an additional indication of the failure to 

successfully dissolve the test solution. Solubility is defined by the Agency’s Pesticide 

Registration Rejection Rate Analysis Document as the amount of chemical retained in the 

supernatant of a conventionally centrifuged sample of test media. Because the test material was 

not adequately dissolved, it was not possible to obtain accurate toxicity endpoint values that 
104

could be used for risk assessment purposes. The details of the studies are demonstrated in the 

table below. 

Marine/Estuarine Fish Toxicity for Mandipropamid 

Species 

(% 

purity) 

96-hour 

LC50 

(ppm a.i.) 

NOAEC 

(ppm 

a.i.) Toxicity 

Category 

MRID 

No. 

Study 

Classification 

Sheepshead 

minnow 

(Cyprinodon 

variegates) 

96.1 

4.5 2.8 Note 1 Undeterminable 

*** 

468001

-03 

Invalid Note 4

Sheepshead 

minnow 

(Cyprinodon 

variegatus) 

96.1 >5.8 mg 

a..i./L 

4.4 Note 2 Undeterminable 

Note 3

468001

-05 Invalid Note 4

Note 1: The NOAEC value, based on mortality and sub-lethal effects, was 2.8 mg a.i/L. Sub-lethal effects (erratic swimming, lying on the 

bottom of the test vessel, and surfacing for unusually long periods of time) were observed in the groups exposed to 4.3 and 6.1 mg a.i./L of 

NOA446510. As no sub-lethal quantitative measurements were reported, the reviewer was unable to determine an EC50 value. 

Note 2: The NOAEC value, based on sub-lethal effects, was 4.4 mg a.i./L. Sub-lethal effects (loss of equilibrium and lethargy) were observed in 

the group exposed to 5.8 mg a.i./L of NOA446510 (Mandipropamid). As no sub-lethal quantitative measurements were taken, the reviewer was 

unable to determine an EC50 value. 

Note 3: Because of the failure of the mean measured concentrations to remain at least 80% of the nominal concentrations, the concentrations in 

which these effects were observed cannot be validated. 

Note 4: The studies were invalidated because of the failure of the study authors to take appropriate measures to ensure the test chemical was 

adequately dissolved in the test water. This was indicated by the failure of the measured concentrations to remain at least 80% of the nominal 

concentrations, as required by the fish acute toxicity Guideline, 850.1075. 

Estuarine and Marine Fish, Chronic 

Currently, no estuarine and marine fish chronic toxicity studies have been submitted to the 

Agency. 

iii. Estuarine and Marine Invertebrates, Acute

Mandipropamid usage may occur in some areas associated with marine/estuarine habitats. Thus, 

marine/estuarine fish toxicity data is required. There are two registrant submitted acute toxicity 

studies testing marine/estuarine invertebrate. The details of the studies are demonstrated in the 

table below. 
105

Freshwater Invertebrate Toxicity for Mandipropamid 

Species 

Chemical 

(% purity). 

96-hour 

EC50 

(ppm a.i.) 

NOAEC 

(ppm 

a.i.;) Toxicity 

Category 

MRID 

No. 

Study 

Classification 

Mysid shrimp 

(Americamysis 

bahia) 

96.1% 1.7(based 

on 

mortality) 

0.58 Moderately 

toxic 

468001

-02 

Acceptable 

Oyster 

Crassostrea 

virginica

96.1 0.91 (based 

on sublethal 

effect of 

shell 

deposition) 

0.46 Very 

Highly 

toxic 

468001

-01 Acceptable 

iv. Estuarine and Marine Invertebrate, Chronic

Currently, no estuarine and marine invertebrate chronic toxicity studies have been submitted to 

the Agency. 

d. Toxicity to Plants 

i. Terrestrial Plants

The registrant submitted a seedling emergence and vegetative vigor study testing the A12946B, 

the formulation containing the active ingredient Mandipropamid. The following summarizes the 

results of both studies. 

The effect of A12946B on the seedling emergence of monocot (corn, Zea mays; oat, Avena 

sativa; onion, Allium cepa; and ryegrass, Lolium perenne) and dicot (carrot, Daucus carota; 

cucumber, Cucumis sativa; radish, Raphanus sativus; soybean, Glycine max; sugar beet, Beta 

vulgaris; and tomato, Lycopersicon esculentum) crops was studied at nominal application rates 

of 0 (negative and surfactant controls), 0.0413, 0.0825, 0.165, 0.330 and 0.660 lbs ai/A. The 

growth medium used in the seedling emergence test was natural soil, classified as a loam soil, 

with an organic matter content of 1.7% (1.0% organic carbon) and an adjusted pH of 7.4. On 

day 21 the surviving plants per pot were recorded and cut at soil level for measuring the plant 

height and dry weight. 

Dry weight was significantly affected in cucumber, soybean and tomato, but reductions did not 

exceed 25%. The % inhibition in seedling emergence in the treated species as compared to the 

control ranged from -4 to 8%. No monocot species was sensitive to treatment, but an EC05 value 

could be calculated for corn dry weight. Carrot was the only dicot species to exhibit a reduction 

of ≥25% (based on dry weight) relative to the negative control; however, the response was not 

dose-dependent, with the three lowest treatment groups experiencing increases in dry weight of 

2-21%. The reviewer was unable to determine reliable ECx values for carrot dry weight. 
106

Additionally, one replicate in the highest treatment group failed to emerge and overall emergence 

of the controls and treatment groups was fairly low (60-73%). This implies that factors other than 

treatment contributed to the poor performance of carrot in this study. The study was deemed 

supplemental because of this study deficiency. 

SEEDLING EMERGENCE STUDY (468001-17) SUMMARY OF MOST SENSITIVE 

PARAMETERS BY SPECIES (LBS AI/A). 

Species Endpoint NOAEC EC05 EC25

EC50

Corn None 0.660 <0.0413 >0.660 >0.660 

Oat None 0.660 >0.660 >0.660 >0.660 

Onion None 0.660 ND >0.660 >0.660 

Ryegrass None 0.660 ND >0.660 >0.660

Carrot Not 

Determinable 

Not 

Determinable

Not 

Determinable

Not 

Determinable

Not 

Determinable

Cucumber None 0.165 <0.0413 >0.660 >0.660

Radish None 0.660 0.36 >0.660 >0.660

Soybean None 0.165 <0.0413 >0.660 >0.660

Sugar beet None 0.660 ND >0.660 >0.660

Tomato None 0.660 ND >0.660 >0.660

The effect of A12946B on the vegetative vigor of monocot (corn, Zea mays; oat, Avena sativa; 

onion, Allium cepa; and ryegrass, Lolium perenne) and dicot (carrot, Daucus carota; cucumber, 

Cucumis sativa; radish, Raphanus sativus; soybean, Glycine max; sugar beet, Beta vulgaris; and 

tomato, Lycopersicon esculentum) crops was studied at nominal application rates of 0 (negative 

and surfactant controls), 0.0495, 0.0994, 0.198, 0.396 and 0.792 lbs ai/A. The growth medium 

used in the test was an artificial soil that represented a loam soil and was composed of a mixture 

of kaolinite clay, industrial quartz sand and peat; the organic matter content was 1.7% (1.0% 

organic carbon) and the pH was 7.4. On day 21 the surviving plants per pot were recorded and 

cut at soil level for measuring the plant height and dry weight. 

In the vegetative vigor test, plant height was affected by A12946B treatment in oat only. Dry 

weight, plant height and survival were not affected in any other species. The most sensitive 

monocot species, based on plant height, in the vegetative vigor test was oat with an EC25 of 

>0.792 lbs ai/A and a NOAEC of 0.198 lbs ai/A. No dicot was sensitive to treatment, so the 

EC25 value was >0.792 lbs ai/A and the NOAEC values was 0.792 lbs ai/A. 

The study was deemed acceptable for a tier II vegetative vigor terrestrial plant toxicity study. 
107

VEGETATIVE VIGOR STUDY (468001-18) SUMMARY OF MOST SENSITIVE 

PARAMETERS BY SPECIES (LBS AI/A). 

Species Endpoint NOAEC EC05 EC25

EC50

Corn None 0.792 >0.792 >0.792 >0.792 

Oat Plant Height 0.198 >0.792 >0.792 >0.792 

Onion None 0.792 >0.792 >0.792 >0.792 

Ryegrass None 0.792 >0.792 >0.792 >0.792 

Carrot None 0.792 >0.792 >0.792 >0.792 

Cucumber None 0.792 >0.792 >0.792 >0.792 

Radish None 0.792 >0.792 >0.792 >0.792 

Soybean None 0.792 >0.792 >0.792 >0.792 

Sugar beet None 0.792 >0.792 >0.792 >0.792 

Tomato None 0.792 >0.792 >0.792 >0.792 
ii. Aquatic Plants 

The registrant has submitted a nonvascular aquatic plant toxicity study testing the effect of 

mandipropamid on Pseudokirchneriella subcapitata, and a vascular aquatic plant toxicity study 

testing the effect of mandipropamid on lemna gibba. The registrant has also submitted a 

nonvascular aquatic plant toxicity study testing the effect of CGA380778, a mandipropamid 

degradate, on Pseudokirchneriella subcapitata. Results of the studies are tabulated below. 

Tier II Mandipropamid Aquatic Plant Toxicity Test 

Test Species 

Test Chemical and 

% purity EC50 (ppm) 

NOEAL or 

EC05 (ppm) 

Endpoint 

Effected 

Study 

Category MRID 

Lemna gibba 

Mandipropamid 

96.1 > 7.9 1.3 (EC05) Biomass Acceptable 468001-19 

Pseudokirchneriella 

subcapitata 

Mandipropamid 

96.5 > 2.5 2.5 (NOEAL) Biomass Acceptable 468001-21 

Pseudokirchneriella 

subcapitata CGA380778 98.2% 16 2.4 Biomass Acceptable 468001-20 

1 
APPENDIX F. The Risk Quotient Method and 

Levels of Concern 

The risks to terrestrial and aquatic organisms are determined based on a method by which risk 

quotients (RQs) are compared with levels of concern (LOCs). This method provides an 

indication of a chemical’s potential to cause an effect in the field from effects observed in 

laboratory studies, when used as directed. Risk quotients are expressed as the ratio of the 

estimated environmental concentration (EEC) to the species-specific toxicity reference value 

(TRV): 

RQ

EEC

TRV =

Units for EEC and TRV should be the same (e.g., μg/L or ppb). The RQ is compared to the LOC 

as part of a risk characterization. Acute and chronic LOCs for terrestrial and aquatic organisms 

are given in recent Agency guidance (USEPA 2004) and summarized in Table F-1 below. 

Table F-1. Level of concern (LOC) by risk presumption category (USEPA 2004) 

Risk Presumption RQ LOC 

Mammals and Birds 

Acute Risk a EEC b/LC50 or LD50/sqft c or LD50/day d 0.5 

Acute Restricted Use e EEC/LC50 or LD50/sqft or LD50/day (or LD50 <50 mg/kg) 0.2 

Acute Endangered Species f EEC/LC50 or LD50/sqft or LD50/day 0.1 

Chronic Risk EEC/NOEC 1 

Aquatic Animals 

Acute Risk EEC g/LC50 or EC50 0.5 

Acute Restricted Use EEC/LC50 or EC50 0.1 

Acute Endangered Species EEC/LC50 or EC50 0.05 

Chronic Risk EEC/NOEC 1 

Terrestrial and Semi-aquatic Plants 

Acute Risk EEC/EC25 1 

Acute Endangered Species EEC/EC05 or NOEC 1 

Aquatic Plants 

Acute Risk EEC h/EC50 1 

Acute Endangered Species EEC g/EC05 or NOEC 1 a

 Potential for acute toxicity for receptor species if RQ > LOC (USEPA 2004). 

b

 Estimated environmental concentration (ppm) on avian/mammalian food items c

 mg/ft2

d

 mg of toxicant consumed per day 

e

 Potential for acute toxicity for receptor species, even considering restricted use classification, if RQ > LOC (USEPA 

2004). 

f

 Potential for acute toxicity for endangered species of receptor species if RQ > LOC (USEPA 2004). 

g

 EEC = ppb or ppm in water 

h

 EEC = lbs a.i./acre 

2 
For acute exposure to terrestrial and aquatic plants, an LOC of 1 is used. Currently the Agency 

does not perform assessments for chronic risk to plants or acute/chronic risks to non-target 

insects. 

For the Tier II aquatic assessment of mandipropamid acute exposure is represented by the 

maximum 24-hour EEC value calculated using PRZM/EXAMS. EECs used to assess acute and 

chronic risk to avian and mammalian species to mandipropamid were calculated using the Tier I 

model T-REX. 

The Agency has developed an Endangered Species Protection Program to identify pesticides 

whose use may cause adverse impacts on endangered and threatened species, and to implement 

mitigation measures that will eliminate the adverse impacts. At present, the program is being 

implemented on an interim basis as described in a Federal Register notice (54 FR 27984–28008, 

July 3, 1989), and is providing information to pesticide users to help them protect these species 

on a voluntary basis. As currently planned, the final program will call for label modifications 

referring to required limitations on pesticide uses, typically as depicted in county-specific 

bulletins or by other site-specific mechanisms as specified by state partners. A final program, 

which may be altered from the interim program, will be described in a future Federal Register 

notice. The Agency is not imposing label modifications at this time. Rather, any requirements for 

product use modifications will occur in the future under the Endangered Species Protection 

Program. 

3 
APPENDIX G. Data Requirments 

Table G-1. Environmental Fate Data Requirements for Mandipropamid 

Guideline 

No. 

Data Requirement MRID No. Study 

Classification 

161-1 Hydrolysis 46800007,8 Acceptable 

161-2 Photodegradation in Water (pH 7) 46800009,10,11,12,13, 14 Acceptable 

161-3 Photodegradation on Soil 4680000 Acceptable 

161-4 Photodegradation in Air No Data 

162-1 Aerobic Soil Metabolism 4680020,21,22,23,24,25,26,27,28 Acceptable 

Supplemental 

Supplemental 

Supplemental 

Supplemental 

Supplemental 

Supplemental 

Supplemental 

Supplemental 

162-2 Anaerobic Soil Metabolism 468000027 Supplemental 

162-3 Anaerobic Aquatic Metabolism 46800033,34 Unacceptable 

162-4 Aerobic Aquatic Metabolism 46800032 Unacceptable 

163-1 Adsorption/Desorption 46800035, 36, 37,38, 

39,40,41,42, 43 

Supplemental 

163-2 Laboratory Volatility No Data 

163-3 Field Volatility No Data 

164-1 Terrestrial Field Dissipation 46800045 Acceptable 

164-2 Aquatic Field Dissipation No Data 

164-3 Forestry Dissipation No Data 

165-4 Accumulation in Fish No Data 

166-1 Ground Water – small prospective No Data 

166-2 Ground Water – small retrospective No Data 

201-1 Droplet Size Spectrum No Data 

202-1 Drift Field Evaluation No Data 

4 
Table G-2. Ecological Effects Data Requirements for Mandipropamid 

Guideline 

No. 

Data 

Requirement Species Formulation 

Are data 

adequate for 

ecological risk 

assessment? 

MRID Number 

(Study 

Classification) 

Anas Platyrhynchos 

(mallard duck) 

Technical Yes 46800110 

(Acceptable) 

71-1 

850.2100 

Avian Acute 

Oral Toxicity 

Colinus virginianu 

(bobwhite quail)

Technical Yes 46800111 

(Acceptable) 

Colinus virginianu 

(bobwhite quail) 

Technical Yes 46800112 

(Acceptable) 

71-2 

850.2200 

Avian Subacute 

Dietary Toxicity 

Anas Platyrhynchos 

(mallard duck)

Technical Yes 46800113 

(Acceptable) 

Colinus virginianu 

(bobwhite quail)

Technical Yes 46800114 

(Acceptable) 

71-4 

850.2300 

Avian 

Reproduction 

Toxicity Anas Platyrhynchos 

(mallard duck)

Technical Yes 46800115 

(Acceptable) 

Pimephales promelas 

(fathead minnow)

Technical No 46800104 

(Unacceptable) 

72-1 

850.1075 

Freshwater Fish 

LC50

Oncorhynchus mykiss

(rainbow trout)

Technical No 46800105 

(Unacceptable) 

72-2 

850.1010 

Freshwater 

Invertebrate 

Acute LC50

Daphnia magna 

(water flea)

Technical Yes 46800150 

(Acceptable) 

72-3(a) 

850.1075 

Estuarine/Marine 

Fish LC50

Cyprinodon 

variegatus 

(sheepshead minnow)

Technical No 46800101 

(Unacceptable) 

72-3(b) 

850.1025 

Estuarine/Marine 

Invertebrate 

(Mollusk) 

Crassostrea virginica

(eastern oyster)

Technical Yes 46800101 

(Acceptable) 

72-3(c) 

850.1035 

850.1045 

Estuarine/Marine 

Invertebrate 

(Mysid)

Americamysis bahia 

(mysid shrimp)

Technical Yes 46800102 

(Acceptable) 

72-4 (a) 

850.1400 

Fish Early 

Life-Stage 

(Freshwater) 

(Marine) 

Pimephales promelas 

(fathead minnow) 

Technical Yes 46800108 

(Acceptable) 

72-4 (b) 

850.1300 

850.1350 

Aquatic 

Invertebrate 

Life-Cycle 

(Freshwater) 

(Marine) 

Americamysis bahia 

(mysid shrimp) 

Technical No data 

submitted 

5 
Table G-2. Ecological Effects Data Requirements for Mandipropamid 

Guideline 

No. 

Data 

Requirement Species 

Are data 

Formulation 

adequate for MRID Number 

ecological risk (Study 

assessment? Classification) 

72-5 

850.1500 

Fish Full LifeCycle 

(Freshwater) 

(Marine) 

No data submitted No data 

submitted 

No – 

122-1(a) 

850.4100 

Seed 

Germination/ 

Seedling 

Emergence 

(Tier I)

No data submitted No data 

submitted 

No – 

122-1(b) 

850.4150 

Vegetative Vigor 

(Tier I) 

No data submitted No data 

submitted 

No – 

122-2 Technical Yes 

850.4400 

Aquatic Plant 

Growth (Tier I) 

Lemna gibba

(duckweed) Technical Yes 

123-1(a) 

850.4225 

Seed 

Germination/ 

Seedling 

Emergence 

(Tier II) 

Monocots and Dicots Formulation c Partially 46800117 

(Supplemental) 

123-1(b) 

850.4250 

Vegetative Vigor 

(Tier II) 

Monocots and Dicots Formulation c Yes 46800118 

(Acceptable) 

123-2 

850.4400 

Aquatic Plant 

Growth (Tier II) 

Lemna gibba 

(duckweed)

Technical Yes 466800119 

(Acceptable) 

Anabaena flos-aquae 

(freshwater alga)

Technical No 

Skeletonema costatum

(marine alga) 

Technical No 

Pseudokirchneriella 

subcapitata 

Technical Yes 46800121 

(Acceptable) 

123-2 

850.5400 

Algal Plant 

Toxicity 

(Tier I and 

Tier II) 

Navicula pelliculosa 

(freshwater alga)

Technical No 

141-1 

850.3020 

Honeybee Acute 

Contact Toxicity 

Test 

Apis mellifera (honey 

bee)

Technical Yes 46800116 

(Supplemental) 

141-2 

850.3030 

Residues on 

Foliage 

Honeybee 

Toxicity Test 

No data submitted No data 

submitted 

No 

NonGuideline Honeybee 

Feeding Toxicity 

Test 

No Data Submitted No data 

submitted 

No 

NonGuideline Benthic 

Organisms 

Chironomus riparius

(midge)

No data 

submitted 

No 

NonGuideline Earthworm 

Subacute 

No No data 

submitted 

No 

6 
APPENDIX H. Use Characterization Maps

There are no madnipropamid use characterization maps available. 

7 
APPENDIX I. Environmental Fate Bibliography

MRID Environmental Fate Studies Submitted to EPA

MRID 46800007 - Buckel, T. 2002. Hydrolysis of [ethyl-1-14C]-labelled NOA446510 under 

laboratory conditions. Unpublished study performed and sponsored by Syngenta Crop 

Protection AG, Basel, Switzerland, and submitted by Syngenta Crop Protection, Inc. 

Greensboro, NC. Basel No.: 02TB01; Syngenta No.: T004591-02. Experiment started April 2, 

2002, and completed May 13, 2002. Final report issued November 8, 2002. 

MRID 46800008 - Murphy, T. 2006. Hydrolysis of [ethyl-1-14C]-labelled NOA446510 under 

laboratory conditions, study profile. Unpublished study summary prepared, sponsored and 

submitted by Syngenta Crop Protection, Inc., Greensboro, North Carolina. Syngenta Study No.: 

T004591-02. Experimental start and termination dates not applicable. Final report issued 

February 24, 2006. 

MRID 46800009- Kuet, S.F. 2004. NOA446510: photolysis of 14C-chlorophenyl ring labelled 

NOA446510 in sterile natural water under laboratory conditions. Unpublished study performed 

by Jealott’s Hill International Research Centre, Berkshire, UK, and submitted and sponsored by 

Syngenta Crop Protection, Inc. Greensboro, NC. Jealott’s Hill No.: RJ3510B; Syngenta No.: 

T004575-02. Experiment started October 2, 2003, and completed January 20, 2004. Final report 

issued November 25, 2004. 

MRID 46800010- Harrison, C.L. 2004. NOA446510: 14C-methoxyphenyl labelled sterile 

natural water photolysis under laboratory conditions. Unpublished study performed by Jealott’s 

Hill International Research Centre, Berkshire, UK, and submitted and sponsored by Syngenta 

Crop Protection, Inc. Greensboro, NC. Jealott’s Hill No.: RJ3481B; Syngenta No.: T004607-02. 

Experiment started November 27, 2003, and completed March 22, 2004. Final report issued 

December 22, 2004. 

MRID 46800011 - Nicollier, G. 2003. Aqueous photolysis of [chlorophenyl-U-14C]-labelled 

NOA446510 under laboratory conditions. Unpublished study performed and sponsored by 

Syngenta Crop Protection AG, Basel, Switzerland, and submitted by Syngenta Crop Protection, 

Inc. Greensboro, NC. Basel No.: 02GN07; Syngenta No.: T004618-02. Experiment started May 

14, 2002, and completed July 01, 2003. Final report issued October 31, 2003. 

MRID 46800012 - Murphy, T. 2006. Aqueous photolysis of [chlorophenyl-U-14C]-labelled 

NOA446510 under laboratory conditions, study profile. Unpublished study summary prepared, 

sponsored and submitted by Syngenta Crop Protection, Inc., Greensboro, North Carolina. 

Syngenta Study No.: T004618-02. Experimental start and termination dates not applicable. 

Final report issued February 23, 2006. 

MRID 46800013 - Hand, L.H. and J. Towers. 2003. Aqueous photolysis of 14C-methoxyphenylNOA446510 under laboratory conditions. Unpublished study performed and sponsored by 

8 
Syngenta Jealott’s Hill International Research Centre, Berkshire, UK and submitted by Syngenta 

Crop Protection, Inc., Greensboro, NC. Study No.: 02JH091; Syngenta No.: T004630-02. 

Experiment started November 20, 2002, and completed May 28, 2003. Final report issued 

August 18, 2003. 

MRID 46800014 - Murphy, T. 2006. Aqueous photolysis of 14C–methoxypehnyl-NOA446510 

under laboratory conditions, study profile. Unpublished study summary prepared, sponsored and 

submitted by Syngenta Crop Protection, Inc., Greensboro, North Carolina. Syngenta Study No.: 

T004630-02. Experimental start and termination dates not applicable. Final report issued 

February 13, 2006. 

MRID 46800015 - Bramley, Y.M. NOA446510: Soil photolysis of 14C-chlorophenyl ring 

labelled NOA446510 under laboratory conditions. Unpublished study performed by Jealott’s 

Hill International Research Centre, Berkshire, UK and sponsored and submitted by Syngenta 

Crop Protection, Inc., Greensboro, NC. Report No.: RJ3535B. Syngenta No.: T008105-03. 

Experiment initiated January 14, 2004 and completed January 7, 2005. Final report issued 

February 7, 2005. 

MRID 46800016: Murphy, T. 2006. NOA446510: Soil photolysis of 14C-methoxyphenyl ring 

labelled NOA446510 under laboratory conditions. Unpublished study sponsored and submitted 

by Syngenta Crop Protection, Inc., Greensboro, NC. Syngenta No.: T004595-02. Experiment 

start and completion date not applicable. Final report issued February 13, 2006. 

9 
MRID 46800017: Kuet, S.F. 2003. NOA446510: Soil photolysis of 14C-methoxyphenyl ring 

labelled NOA446510 under laboratory conditions. Unpublished study performed by Jealott’s 

Hill International Research Centre, Berkshire, UK and sponsored and submitted by Syngenta 

Crop Protection, Inc., Greensboro, NC. Jealott’s Hill No.: RJ3400B. Syngenta No.: T004595-

02. Study started January 8, 2003 and completed August 20, 2003. Final report issued 

December 10, 2003. 

MRID 46800016: Murphy, T. 2006. NOA446510: Soil photolysis of 14C-methoxyphenyl ring 

labelled NOA446510 under laboratory conditions. Unpublished study sponsored and submitted 

by Syngenta Crop Protection, Inc., Greensboro, NC. Syngenta No.: T004595-02. Experiment 

start and completion date not applicable. Final report issued February 13, 2006. 

MRID 46800018: McKillican, C. B. 2005. Photodegradation of 14C-NOA-446510 on soil under 

artificial light. Unpublished study performed, sponsored and submitted by Syngenta Crop 

Protection, Inc., Greensboro, NC. Syngenta No.: 737-02. Study started June 15, 2004 and 

completion date not reported . Final report issued July 29, 2005. 

MRID 46800019: Murphy, T. 2006. Photodegradation of 14C-NOA-446510 on soil under 

artificial light. Unpublished study sponsored and submitted by Syngenta Crop Protection, Inc., 

Greensboro, NC. Syngenta No.: 000737-02. Experiment start and completion date not 

applicable. Final report issued February 13, 2006. 

MRID 46800020: Clark, A. 2004. Metabolism of [14C-chlorophenyl]-NOA-446510 in viable 

soil under aerobic conditions. Unpublished study performed, submitted and sponsored by 

Syngenta Crop Protection, Inc, Greensboro, NC. Study No.: T000680-02. Syngenta No.: 680-

02. Experiment started March 7, 2003. Experimental completion date not reported. Final report 

issued September 1, 2004. 

MRID 46800021: Murphy, T. 2006. Metabolism of [14C-chlorophenyl]-NOA-446510 in viable 

soil under aerobic conditions. Unpublished study submitted and sponsored by Syngenta Crop 

Protection, Inc, Greensboro, NC. Syngenta No.: T000680-02. Experiment start and completion 

date not applicable. Final report issued February 13, 2006. 

MRID 46800022: Nicollier, G. 2003. Metabolism of [methoxyphenyl-U-14C] labelled 

NOA446510 under aerobic, aerobic/anaerobic and sterile aerobic laboratory conditions in one 

soil at 20°C. Unpublished study performed by Syngenta Crop Protection AG, Basel, 

Switzerland, and submitted and sponsored by Syngenta Crop Protection, Inc., Greensboro, NC. 

Basel Number: 02RF02. Syngenta Number: T004633-02. Experiment initiated on June 6, 2002 

and completed on November 28, 2003. Final report issued on December 18, 2003.

MRID 46800023: Berdat, T. 2005. Rate of degradation of [14C] CGA380778 (metabolite of 

NOA446510) in various soils under aerobic laboratory conditions at 20°C. Unpublished study 

performed and sponsored by Syngenta Crop Protection AG, Basel, Switzerland and submitted by 

Syngenta Crop Protection, Inc., Greensboro, NC. Sygenta No.: T004943-04. Experiment started 

August 4, 2004 and completed January 20, 2005. Final report issued March 13, 2005. 

10 
MRID 46800024: Hand, L.H. 2004. NOA446510: Rate of degradation in one soil under 

various laboratory conditions. Unpublished study performed by Jealott’s Hill International 

Research Centre, Berkshire, UK and submitted and sponsored by Syngenta Crop Protection, Inc, 

Greensboro, NC. Report No.: RJ3487B. Syngenta No.: T008097-03. Experiment started July 7, 

2003 and completed February 27, 2004. Final report issued July 14, 2004. 

MRID 46800025: Murphy, T. 2006. NOA446510: Rate of degradation in one soil under 

various laboratory conditions. Unpublished study submitted and sponsored by Syngenta Crop 

Protection, Inc., Greensboro, NC. Syngenta No.: T008097-03. Experiment start and completion 

date not applicable. Final report issued February 13, 2006. 

MRID 46800026: Dorn, R., A. Clark, J. Perine, W. Chen, and T. Murphy. 2006. Evaluation of 

degradation times after adjustment for temperature and moisture effects of NOA446510 and its 

metabolite in various soils under laboratory conditions. Unpublished summary report prepared, 

sponsored and submitted by Syngenta Crop Protection, Inc., Greensboro, North Carolina. 

Syngenta Study No.: T014422-05. Experimental start date and termination date not applicable. 

Final report issued March 1, 2006. 

MRID 46800027: Nicollier, G. 2003. Metabolism of [chlorophenyl-U-14C] labelled 

NOA446510 under aerobic and aerobic/anaerobic laboratory conditions in one soil at 20°C. 

Unpublished study performed by Syngenta Crop Protection AG, Basel, Switzerland, submitted 

and sponsored by Syngenta Crop Protection, Inc., Greensboro, NC. Basel Number: 02TB03; 

Syngenta Number: T004572-02. Experiment initiated on July 16, 2002 and completed on 

January 7, 2003 (p. 9). Final report issued on November 6, 2003. 

MRID 46800028: Kuet, S.F. NOA446510: Metabolism and rate of degradation of 14Cchlorophenyl ring labelled NOA446510 under aerobic laboratory conditions, in three soils, at 

20°C. Unpublished study performed by Jealott’s Hill International Research Centre, Berkshire, 

UK and submitted and sponsored by Syngenta Crop Protection, Inc, Greensboro, NC. Report 

No.: RJ3469B. Syngenta No.: T008109-03. Experiment started March 27, 2003 and completed 

December 3, 2003 (p. 28). Final report issued July 16, 2004. 

MRID 46800029: Dorn, R. 2005. Evaluation of half-lives of selected metabolites of 

NOA446510 in aquatic systems. Unpublished summary report prepared, sponsored and 

submitted by Syngenta Crop Protection, Inc., Greensboro, North Carolina. Syngenta Study No.: 

T001209-06 and Report No.: Ass05RD04 (pp. 1, 4). Experimental start date and termination 

date not applicable. Final report issued August 16, 2005. 

MRID 46800030: Murphy, T. 2006. NOA446510: degradation in two aquatic sediment 

systems, study profile. Unpublished study summary prepared, sponsored and submitted by 

Syngenta Crop Protection, Inc., Greensboro, North Carolina. Syngenta Study No.: T008095-03. 

Experimental start and termination dates not applicable. Final report issued March 9, 2006. 

11 
MRID 46800031: Hurt, A.D. 2005. NOA446510: degradation on two aquatic sediment 

systems, final report. Unpublished study performed by Jealott's Hill International Research 

Centre, Berkshire, United, Kingdom, sponsored and submitted by Syngenta Crop Protection, 

Inc., Greensboro, North Carolina. JH Study No.: 03JH023 and Report No.: RJ3669B (pp. 1, 15 

in MRID 46800031). Syngenta Study No.: T008095-03. Experimental start date July 16, 2003, 

and termination date February 24, 2005 (p. 50 in MRID 4600031). Final report issued July 27, 

2005. 

MRID 46800032: Oliver, R.G., et al. 2005. NOA446510: degradation in an outdoor aquatic 

sediment system. Unpublished study performed by Jealott's Hill International Research Centre, 

Berkshire, United Kingdom, sponsored and submitted by Syngenta Crop Protection, Inc., 

Greensboro, North Carolina. JH Study No.: 04JH007 and Report No.: RJ3569B (pp. 1, 12). 

Syngenta Study No.: T009117-04. Experimental start date June 2, 2004, and termination date 

May 10, 2005 (p. 35). Final report issued July 27, 2005. 

MRID 46800033: Hurt, A.D. 2005. NOA446510: degradation in two aquatic sediment systems 

(methoxyphenyl ring), final report. Unpublished study performed by Jealott's Hill International 

Research Centre, Berkshire, United Kingdom, sponsored and submitted by Syngenta Crop 

Protection, Inc., Greensboro, North Carolina. JH Study No.: 03JH035 and Report No.: RJ3580B 

(pp. 1, 6 in MRID 46800033). Syngenta Study No.: T008104-03. Experimental start date May 

6, 2004, and termination date April 13, 2005 (p. 43 in MRID 4600033). Final report issued July 

14, 2005. 

MRID 46800034: Clark, A. 2006. NOA446510: degradation on two aquatic sediment systems 

(methoxyphenyl ring), study profile. Unpublished study summary prepared, sponsored and 

submitted by Syngenta Crop Protection, Inc., Greensboro, North Carolina. Syngenta Study No.: 

T008104-03. Experimental start and termination dates not applicable. Final report issued March 

3, 2006. 

MRID 46800035: Indergand, P. 2005. Adsorption/desorption of a [chlorophenyl-U-14C]-

labeled SYN521195 in various soils. Unpublished study performed and sponsored by Syngenta 

Crop Protection AG, Bracknell, Basel, Switzerland; submitted by Syngenta Crop Protection Inc., 

Greensboro, North Carolina. Syngenta Number T013384-04. Experimental start date January 

27, 2005, and experimental completion date June 21, 2005 (p. 9). Study completion date August 

19, 2005. 

MRID 46800036: Hand, L.H. and E.A. Fleming. 2005. Adsorption/desorption properties of a 

metabolite (SYN539678) in three soils. Unpublished study performed by Jealott’s Hill 

International Research Centre, Bracknell, Berkshire, United Kingdom; submitted and sponsored 

by Syngenta Crop Protection Inc., Greensboro, North Carolina. Syngenta Number T013385-04. 

Jealott’s Hill Number RJ3674B. Experimental start date January 11, 2005, and experimental 

completion date May 11, 2005 (p. 22). Study completion date July 6, 2005. 

MRID 46800037: Indergand, P. and G. Nicollier. 2005. Adsorption/desorption of [phenyl-U14C]-labeled SYN500003 in various soils (including final report amendment 1). Unpublished 

12 
study performed and sponsored by Syngenta Crop Protection AG, Basel, Switzerland; submitted 

by Syngenta Crop Protection Inc., Greensboro, North Carolina. Syngenta Number T0006595-04. 

Experimental start date January 11, 2005, and experimental completion date May 2, 2005 (p. 9). 

Study completion date June 9, 2005. 

MRID 46800038: Nicollier, G. 2003. Adsorption/desorption of [methoxyphenyl-U-14C]-

labelled NOA446510 in various soils (including final report amendment 1). Unpublished study 

performed and sponsored by Syngenta Crop Protection AG, Basel, Switzerland; and submitted 

by Syngenta Crop Protection Inc., Greensboro, NC. Syngenta AG Study Number T004577-02. 

Basel Number 02TB04. Experimental start date August 9, 2002, and completion date February 

18, 2002 (p. 9). Final report issued October 24, 2003. 

MRID 46800039: Murphy, T. 2006. Adsorption/desorption of [methoxyphenyl-U-14C]-labelled 

NOA446510 in various soils. Unpublished study submitted and sponsored by Syngenta Crop 

Protection Inc., Greensboro, NC. Syngenta Study Number T004577-02. Study completion date 

February 27, 2006. 

MRID 46800040: Berdat, T. and G. Nicollier. 2004. NOA446510: Adsorption/desorption of 

[methoxyphenyl-U-14C]-labelled NOA446510 in various US field soils (includes final report 

amendment 1). Unpublished study performed by Syngenta Crop Protection AG, Basel, 

Switzerland; sponsored and submitted by Syngenta Crop Protection Inc., Greensboro, North 

Carolina. Study Number 04TB01. Syngenta Number T000738-02. Experimental start date 

January 16, 2004, and experimental completion date March 17, 2004 (p. 9). Study completion 

date December 23, 2004. 

MRID 46800041: Murphy, T. 2006. NOA446510: Adsorption/desorption of [methoxyphenylU-14C]-labelled NOA446510 in various US field soils. Sponsored and submitted by Syngenta 

Crop Protection Inc., Greensboro, North Carolina. Syngenta Number T000738-02. Completion 

date March 8, 2006. 

MRID 46800042: Adam, D. 2004. Adsorption/desorption of [14C]-CGA380778 on various 

soils. Unpublished study performed by RCC Ltd, Itingen, Switzerland; sponsored and submitted 

by Syngenta Crop Protection Inc., Greensboro, North Carolina. RCC Study Number 855381. 

Syngenta Number T004956-04. Experimental start date August 11, 2004, and completion date 

September 22, 2004 (p. 12). Study completion date December 6, 2004. 

MRID 46800043: Murphy, T. 2006. Adsorption/desorption of [14C]-CGA380778 on various 

soils. Sponsored and submitted by Syngenta Crop Protection Inc., Greensboro, North Carolina. 

Syngenta Number T004956-04. Study completion date March 8, 2006. 

MRID 46800044: Harrison, C.L. 2005. NOA446510: Adsorption/desorption properties of a 

water sediment metabolite SYN504851 in three soils. Unpublished study performed by Jealott’s 

Hill International Research Centre, Bracknell, Berkshire, United Kingdom; submitted and 

sponsored by Syngenta Crop Protection Inc., Greensboro, North Carolina. Syngenta Number 

13 
T013383-04. Jealott’s Hill Number RJ3633B. Experimental start date January 5, 2005, and 

experimental completion date April 1, 2005 (p. 20). Study completion date May 19, 2005. 

MRID 46800045: Peters, J. 2005. Dissipation of NOA446510 250SC in bare soil plot under 

simulated leafy vegetable production conditions in the San Joaquin Valley of California. 

Unpublished study performed by Syngenta Crop Protection, Inc., Greensboro, NC; Excel 

Research Services, Inc., Fresno, CA (field research facility); and North Coast Laboratories, Ltd., 

Arcata, CA (analytical laboratory); and sponsored and submitted by Syngenta Crop Protection, 

Inc., Greensboro, NC. Syngenta No. T000052-03. Excel Study No. ERS23039. NCL No. 

110.025. Experiment initiation October 1, 2003 (first application date; Appendix 1, p. 84) and 

completion April 29, 2005 (analytical phase termination date; Appendix 2, p. 133). Final report 

issued October 3, 2005. 

MRID 46800046: Peters, J. 2005. Dissipation of NOA446510 250SC under field conditions on 

crop (potatoes) and bare soil in New York. Unpublished study performed by Syngenta Crop 

Protection, Inc., Greensboro, NC; Waterborne Environmental, Inc., Leesburg, VA (field phase 

management); A.C.D.S. Research , Inc., North Rose, NY (field research facility); and EnviroTest Laboratories, Edmonton, Alberta, Canada (analytical laboratory); and sponsored and 

submitted by Syngenta Crop Protection, Inc., Greensboro, NC. Syngenta No. T000053-03. ETL 

Report No. 05SYN150.REP. WEI Study No. 242.68. Experiment initiation August 7, 2003 (first 

application date; Appendix 1, p. 93) and completion February 24, 2005 (analytical phase 

termination date; Appendix 2, p. 199). Final report issued October 3, 2005. 

MRID 46800047: Peters, J. 2005. Dissipation of NOA446510 250SC in a bare soil plot under 

simulated squash production conditions in Georgia. Unpublished study performed by Syngenta 

Crop Protection, Inc., Greensboro, NC (analytical laboratory); Waterborne Environmental, Inc., 

Leesburg, VA (field management); Ag. Research Associates, LLC, Chula, GA (field research 

facility); and sponsored and submitted by Syngenta Crop Protection, Inc., Greensboro, NC. 

Syngenta No. T000054-03. WEI Study No. 242.69. Experiment initiation May 21, 2003 (first 

application date; Appendix 1, p. 78) and completion July 13, 2005 (analytical phase; Appendix 2, 

p. 165). Final report issued October 3, 2005. 

MRID 46800109: Roberts, G.C. and F. Peurou. 2003. NOA446510: Determination of the 

accumulation and elimination of [14C]NOA446510 in fathead minnow (Pimephales promelas). 

Unpublished study performed by Brixham Environmental Laboratory, United Kingdom; 

sponsored and submitted by Syngenta Crop Protection, Inc., Greensboro, NC. Brixham Number 

BL7579/B. Syngenta Number T011831-05. Experiment initiated March 12, 2003, and 

completed May 30, 2003 (p. 10). Final report issued December 18, 2003. 

14 
MRID 46800048 (NG study): Peters, J. and B. Schwartz. 2005. Stability of NOA-446510 and 

CGA-380778 in soil under freezer storage conditions. Unpublished study performed and 

sponsored and submitted by Syngenta Crop Protection, Inc., Greensboro, NC. Syngenta No. 

T001672-03. Experiment initiation November 24, 2003 and completion September 9, 2005 (p. 8 

and Appendix 1, p. 68). Final report issued November 7, 2005. 

MRID 46800049 (NG study): Chen, W. 2006. Degradation of NOA446510 influenced by soil 

temperature under cropped and bare soil conditions: A conceptual model approach to bridge data 

from laboratory to field. Unpublished summary report prepared, sponsored, and submitted by 

Syngenta Crop Protection, Inc., Greensboro, North Carolina. Syngenta Study No.: T021955-04. 

Experimental start date and termination date not applicable. Final report issued March 22, 2006. 

MRID 46800124 (NG study): Kendall, T. and W. Nixon. 2005. Analytical method 

verification for the determination of NOA446510 in saltwater. Unpublished study performed by 

Wildlife International, Ltd., Easton, Maryland, sponsored and submitted by Syngenta Crop 

Protection, Inc., Greensboro, North Carolina. Wildlife International Project No.: 528C-123 (p. 

8). Syngenta Study No.: T003405-03. Experimental start and termination date November 15, 

2004 (p. 8). Final report issued May 13, 2005. 

MRID 46800125 (NG study): Bruns, G. and S. Nelson. 2004. Independent laboratory 

validation: Syngenta: “Analytical method REM 202.02 for the determination of NOA-446510 

and its metabolite CGA-380778, in soil, using liquid chromatography-electrospray ionization 

tandem mass spectrometry (including validation data).” Unpublished study performed by 

Enviro-Test Laboratories, Edmonton, Alberta, Canada, sponsored and submitted by Syngenta 

Crop Protection, Inc., Greensboro, North Carolina. ETL Study No.: 04ILV05SYN and Report 

No.: 04SYN142.REP. Syngenta Study No.: T006443-04. Experimental start and termination 

dates not reported; study initiation date September 17, 2004 (p. 8). Final report issued November 

23, 2004. 

MRID 46800126 (NG study): Williams, R. 2003. Analytical method REM 202.02 for the 

determination of NOA-446510 and its metabolite CGA-380778, in soil, using liquid 

chromatography-electrospray ionization tandem mass spectrometry (including validation data). 

Unpublished study performed, sponsored and submitted by Syngenta Crop Protection, Inc., 

Greensboro, North Carolina. Syngenta Study No.: T000056-03. Experimental start date not 

reported; study initiation date August 11, 2003 (p. 8). Experimental termination date September 

9, 2003 (p. 8). Final report issued October 9, 2003. 

15 
APPENDIX J. Ecological Toxicity Bibliography

MRID Ecotoxicity Studies Submitted to EPA

MRID 468001-01 Palmer, S.J., et al., NOA446510: A 96-Hour Flow-Through Shell Deposition 

Test with the Eastern Oyster (Crassostrea virginica) Study Completion Date: May 9, 2005 

Wildlife International, Ltd., Easton, MD Syngenta Crop Protection, Greensboro, NC 

MRID 468001-02 Palmer, Susan J., et al. NOA446510: A 96-Hour Flow-Through Acute 

Toxicity Test with the Saltwater Mysid (Americamysis bahia) May 10, 2005 Wildlife 

International, Ltd., Easton, MD Sponsor: Syngenta Crop Protection, Inc., Greensboro, NC 

Laboratory Report ID: 528A-137 MRID No.:468001-02 

MRID 468001-03 Palmer, Susan J., et al. 2005. NOA446510: A 96-Hour Flow-Through Acute 

Toxicity Test with the Sheepshead Minnow (Cyprinodon variegatus). Unpublished study 

performed by Wildlife International, Inc., Easton, MD. Laboratory report number 528A-138. 

Study sponsored by Syngenta Crop Protection, Inc., Greensboro, NC. Study completed May 9, 

2005. 

MRID 468001-04 Maynard, S.J. and R.H. Swarbrick. 2005. NOA446510 Metabolite 

(CGA380778): Acute Toxicity to Rainbow Trout (Oncorhynchus mykiss). Unpublished study 

performed by Brixham Environmental Laboratory, Brixham, Devon TQ5 8BA, UK. Laboratory 

number BL7958/B. Study sponsored by Syngenta Crop Protection, Inc. Study completed 

January 4, 2005. 

MRID 468001-05 Palmer, S.J., et al. 2006. NOA446510: A 96-Hour Flow-Through Acute 

Toxicity Test with the Fathead Minnow (Pimephales promelas). Unpublished study performed 

by Wildlife International, Ltd., Easton, MD. Laboratory report number 528A-146. Stud 

sponsored by Syngenta Crop Protection, Inc., Greensboro, NC. Study completed March 7, 2006. 

MRID 468001-06 Palmer, S.J., et al. 2006. NOA446510: A 96-Hour Flow-Through Acute 

Toxicity Test with the Rainbow Trout (Oncorhynchus mykiss). Unpublished study performed by 

Wildlife International, Inc., Easton, MD. Laboratory report number 528A-147. Study sponsored 

by Syngenta Crop Protection, Inc., Greensboro, NC. Study completed March 7, 2006. 

MRID 468001-07 Grade, R. 2003. Daphnia magna Reproduction Test: Effects of NOA 

446510 on the Reproduction of the Cladoceran Daphnia magna STRAUS in a Semi-Static 

Laboratory Test. Unpublished study performed by Ecological Sciences, Basel, Switzerland. 

Laboratory Study No. 2013604. Study sponsored by Syngenta Crop Protection, Inc., 

Greensboro, NC. Study initiated July 31, 2001 and submitted March 24, 2003. 

MRID 468001-08 Maynard, S.J. 2003. NOA 446510 tech: Early-Life Stage Toxicity Test to 

the Fathead Minnow (Pimephales promelas). Unpublished study performed by Brixham 

16 
Environmental Laboratory, Devon, UK. Laboratory Project No. BL7577/B. Study submitted by 

Syngenta Crop Protection, Inc., Greensboro, NC. Study initiated May 12, 2003 and submitted 

December 22, 2003. 

MRID 468001-09 Gallagher, S.P., L.R. Mitchell, and J.B. Beavers. 2002. NOA446510 

(AMS): An Acute Oral Toxicity Study with the Northern Bobwhite. Unpublished study 

performed by Wildlife International Ltd., Easton, MD. Laboratory Project No. 528-141. Study 

submitted by Syngenta Crop Protection, Inc., Greensboro, NC. Study initiated May 15, 2002 and 

submitted December 11, 2002. 

MRID 468001-10 Gallagher, S.P., and J.B. Beavers. 2005. NOA446510 (AMS): An Acute 

Oral Toxicity Study with the Mallard. Unpublished study performed by Wildlife International 

Ltd., Easton, MD. Laboratory Project No. 528-142. Study submitted by Syngenta Crop 

Protection, Inc., Greensboro, NC. Study initiated May 15, 2002 and submitted July 18, 2005. 

MRID 468001-11 Gallagher, S.P., et al. 2002. NOA446510 (AMS): A Dietary LC50 Study 

with the Mallard. Unpublished study performed by Wildlife International, Ltd., Easton, MD. 

Laboratory Project No. 528-140. Study submitted by Syngenta Crop Protection, Inc., 

Greensboro, NC. Study initiated May 15, 2002 and submitted December 12, 2002. 

MRID 468001-12 Gallagher, S.P., et al. 2002. NOA446510 (AMS): A Dietary LC50 Study 

with the Northern Bobwhite. 

MRID 468001-13 Gallagher, S.P., et al. 2002. NOA446510 (AMS): A Dietary LC50 Study 

with the Northern Bobwhite. Unpublished study performed by Wildlife International, Ltd., 

Easton, MD. Laboratory Project No. 528-139. Study submitted by Syngenta Crop Protection, 

Inc., Greensboro, NC. Study initiated May 15, 2002 and submitted December 11, 2002. 

MRID 468001-14 Frey, L.T., et al. 2003. NOA446510 (AMS): A Reproduction Study with the 

Mallard. Unpublished study performed by Wildlife International Ltd., Easton, MD. Laboratory 

Project No. 528-150. Study submitted by Syngenta Crop Protection, Inc., Greensboro, NC. 

Study initiated August 12, 2002 and submitted June 13, 2003. 

MRID 468001-15 Frey, L.T., et al. 2003. NOA446510 (AMS): A Reproduction Study with the 

Northern Bobwhite. Unpublished study performed by Wildlife International Ltd., Easton, MD. 

Laboratory Project No. 528-149. Study submitted by Syngenta Crop Protection, Inc., 

Greensboro, NC. Study initiated August 12, 2002 and submitted June 13, 2003. 

MRID 468001-16 Dr. C. Grimm, Acute Contact and Oral Toxicity of NOA446510 to Honey 

Bees (Apis mellifera L.) June 03, 2002 Laboratory: Syngenta Crop Protection AG, Ecological 

Sciences, CH-4002 Basel, Switzerland Syngenta Crop Protection, Greensboro, NC Laboratory 

Report ID:2013603 (Basel); T011807-05 (Syngenta) 

MRID 468001-17 Porch, John R., et al. 2005. NOA446510: A Glasshouse Toxicity Study to 

Determine the Effects of a 250 g ai/Litre SC Formulation (A12946B) on the Seedling Emergence 

of Ten Species of Plants. Unpublished study performed by Wildlife International, Ltd., Easton, 

MD. Laboratory report number 528-192. Study sponsored by Syngenta Crop Protection, Inc., 

Greensboro, NC. Study completed October 21, 2005. 

17 
18 

MRID 468001-18 Porch, John R., W. Krip and H.O. Krueger. 2005. NOA446510: A 

Glasshouse Toxicity Study to Determine the Effects of a 250 g ai/Litre SC Formulation 

(A12946B) on the Vegetative Vigor on Ten Species of Plants. Unpublished study performed by 

Wildlife International, Ltd., Easton, MD. Laboratory report number 528-193. Study sponsored 

by Syngenta Crop Protection, Inc., Greensboro, NC. Study completed August 12, 2005. 

MRID 468001-19 Desjardins, D., et al. 2006. NOA446510: A 7-Day Static-Renewal Toxicity 

Test with Duckweed (Lemna gibba G3). Unpublished study performed by Wildlife 

International, Ltd., Easton, MD. Laboratory report number 528A-148. Study sponsored by 

Syngenta Crop Protection, Inc., Greensboro, NC. Study completed March 7, 2006. 

MRID 468001-20 Maynard, S.J. and R.H. Swarbrick. 2005. NOA446510 Metabolite 

(CGA380778): Toxicity to the Green Alga Pseudokirchneriella subcapitata (Formerly 

Selenastrum capricornutum). Unpublished study performed by Brixham Environmental 

Laboratory, UK. Laboratory report number BL7960/B. Study sponsored by Syngenta Crop 

Protection, Inc., Greensboro, NC. Study completed on January 4, 2005. 

MRID 468001-21 Volz, Ernst. 2005. Mandipropamid (NOA446510): Toxicity to 

Pseudokirchneriella subcapitata (formerly Selenastrum capricornutum) in a 96-hour Algal 

Growth Inhibition Test. Unpublished study performed by Environmental Chemistry and 

Pharmanalytics, RCC Ltd., Switzerland. Laboratory study number A33175. Study sponsored by 

Syngenta Crop Protection, Inc., Greensboro, NC. Study completed December 15, 2005. 

MRID 468001-22 Friedrich, Sabine. 2004. CGA380778 (Metabolite of NOA446510): Acute 

Toxicity to the Earthworm Eisenia fetida. Unpublished study performed by BioChem agrar, 

Laboratory for Biological and Chemical Analysis, Ltd., Germany. Laboratory report number 04 

10 48 068. Study sponsored by Syngenta Crop Protection, Inc., Greensboro, NC (Syngenta 

Number T006608-04). Study completed November 16, 2004. 

MRID 468001-23 Friedrich, Sabine. 2001. Acute Toxicity of NOA446510 to the Earthworm 

Eisenia fetida. Unpublished study performed by BioChem agrar, Laboratory for Biological and 

Chemical Analysis, Ltd., Germany. Laboratory report number 01 10 48 060. Study sponsored 

by Syngenta Crop Protection, Inc., Greensboro, NC. Study completed October 29, 2001.