UNITED STATES ENVIRONMENTAL PROTECTION AGENCY

WASHINGTON D.C., 20460

OFFICE OF CHEMICAL SAFETY

AND POLLUTION PREVENTION

PC Code: 115001

DP Barcode: D409249

MEMORANDUM Date: August 27, 2014

Subject: Registration Review: Draft Ecological Risk Assessment and Endangered 

Species Effects Determination for Debacarb

To:

Roy Johnson, Chemical Review Manager

Jill Bloom, Team Leader

Linda Arrington, Branch Chief

Risk Management and Implementation Branch V

Pesticide Re-evaluation Division (7508P)

From: Scott Glaberman, Ph.D., Biologist

Environmental Risk Branch IV

Environmental Fate and Effects Division (7507P)

Reviewed By: Thomas Steeger, Ph.D., Senior Science Advisor

Jim Carleton, Ph.D., Senior Fate Scientist

Environmental Risk Branch IV

Environmental Fate and Effects Division (7507P)

Approved By: Sarah Winfield, Acting Branch Chief

Environmental Risk Branch IV

Environmental Fate and Effects Division (7507P)

The Environmental Fate and Effects Division (EFED) has completed the preliminary ecological 

risk assessment and endangered species effects determination for the benzimidazole carbamate 

fungicide debacarb (first registered in 1982). The only currently registered use of debacarb is as a 

tree injection to ornamental trees in which the compound is distributed systemically throughout 

the tree. 

Since debacarb is used exclusively as a tree injection and is used to treat a low number of estimated 

trees per year across the U.S., the potential for exposure to aquatic receptors as well as non-target 

terrestrial plants is expected to be minimal. Although there is some uncertainty in the potential for 

exposure to aquatic systems from the shedding of leaves from trees treated with debacarb, EFED 

believes that potential risks to these systems may be reduced via use restrictions.

In terms of potential risks of debacarb to terrestrial animals (i.e., birds, mammals, reptiles, 

terrestrial-phase amphibians, and terrestrial invertebrates), there is a limited hazard dataset to carry

out quantitative risk assessment. However, based on a conservative risk analysis performed using 
a composite dataset of debacarb and carbendazim (a carbamate fungicide with a similar structure), 

usage of debacarb is not expected to result in risks of concern to birds (or to terrestrial-phase 

amphibians and reptiles for which birds serves as a surrogate) and mammals. 

There is uncertainty surrounding potential risks of debacarb and its end-use products to insect 

pollinators. Debacarb is systemic, and may be translocated to pollen and nectar of treated trees, 

indicating that exposure to honeybees (Apis mellifera) or other insect pollinators is possible

through ingestion of residues in pollen/nectar. Since no toxicity data are available for honeybees 

exposed to debacarb, it is not possible to rule out the potential for risks of concern to insect 

pollinators. While a relatively low number of trees are estimated to be treated with debacarb each 

year across the U.S., the magnitude of this uncertainty, in part, depends on whether groups of trees 

are treated in close proximity to each other, at similar times, and during parts of the year when 

residues are more likely to be translocated to pollen or nectar, all of which would be more likely 

to result in exposure. It should be noted that data were previously recommended on the fate, uptake, 

and translocation of debacarb in order to estimate potential exposures to insect pollinators 

(USEPA, 2008), but were not submitted. It is also important to note that two of the formulated 

products containing debacarb (i.e., Imisol® and Abasol®) contain the systemic insecticides

imidacloprid (CAS No. 138261-41-3) and avermectin (CAS No. 71751-41-2), respectively, which

are highly toxic to honeybees on an acute exposure basis. The current label for Abasol® indicates 

that the product should only be used as a post-bloom application, while the labels for Imisol® and 

Fungisol® do not have any application restrictions relative to bloom. EFED believes that use

restrictions could potentially reduce the uncertainty and risks associated with the exposure of 

pollinators to residues in pollen and nectar.

There is also uncertainty surrounding potential risks of debacarb and its end-products to terrestrial 

invertebrates in general since some species may consume various edible plant parts containing 

translocated residues (e.g., leaves, fruit) and since there are no available toxicity data for debacarb 

for any species of terrestrial invertebrate.

Since direct adverse effects are not expected for birds, reptiles, terrestrial-phase amphibians, 

mammals, or terrestrial plants, the EPA makes a No Effects (NE) determination for all Federallylisted species within these groups and a No Habitat Modification determination for all designated 

critical habitats associated with these species for the currently registered uses of debacarb. Risks 

to listed aquatic organisms from the use of debacarb may potentially be mitigated via label 

amendment, but effects and habitat modification determinations cannot be made at this time. Risks 

of concern cannot be precluded for listed terrestrial invertebrates, so effects and habitat 

modification determinations also cannot be made at this time.
1

REGISTRATION REVIEW

Draft Ecological Risk Assessment and Endangered Species Effects Determination for:

Debacarb (2-EEEBC)

(CAS Reg. No. 62732-91-6; USEPA PC Code # 115001)

2-(2-ethoxyethoxy) ethyl-2-benzimidazole carbamate

Prepared by:

Scott Glaberman, Ph.D., Biologist

Reviewed by:

Thomas Steeger, Ph.D., Senior Science Advisor

Jim Carleton, Ph.D., Senior Fate Scientist

U. S. Environmental Protection Agency

Office of Pesticide Programs

Environmental Fate and Effects Division

Environmental Risk Branch 3

1200 Pennsylvania Ave., NW

Mail Code 7507P

Washington, DC 20460

August 27, 2014

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2

TABLE OF CONTENTS

1. PROBLEM FORMULATION ........................................................................ 3

Nature of Regulatory Action....................................................................................................... 3

Previous Assessments................................................................................................................. 3

2. STRESSOR SOURCE AND DISTRIBUTION.............................................. 3

Pesticidal Mechanism of Action................................................................................................. 3

Overview of Pesticide Use and Usage........................................................................................ 3

Environmental Fate and Transport ............................................................................................. 5

3. RECEPTORS.................................................................................................... 5

Ecological Effects....................................................................................................................... 5

Ecological Incidents.................................................................................................................... 8

4. ASSESSMENT ENDPOINTS.......................................................................... 8

5. CONCEPTUAL MODEL ................................................................................ 8

Risk Hypothesis.......................................................................................................................... 9

Conceptual Diagram ................................................................................................................... 9

6. ANALYSIS ...................................................................................................... 11

Stressors of Concern ................................................................................................................. 11

Measures of Exposure............................................................................................................... 11

Measures of Effect.................................................................................................................... 13

Integration of Exposure and Effects ......................................................................................... 14

7. RISK CHARACTERIZATION..................................................................... 15

Risk Estimation......................................................................................................................... 15

8. ENDANGERED SPECIES ASSESSMENT................................................. 18

9. ENDOCRINE DISRUPTOR SCREENING PROGRAM........................... 19

10. REFERENCES................................................................................................ 19
3

1. PROBLEM FORMULATION

Nature of Regulatory Action

As part of the implementation of the Registration Review program pursuant to Section 3(g) of 

FIFRA, the Agency is evaluating all current and active registrations for debacarb (2-(2-

ethoxyethoxy) ethyl-2-benzimidazole carbamate) to determine whether it continues to meet the 

FIFRA standard for registration. The structure of this risk assessment is based on guidance 

contained in U.S. EPA’s Guidance for Ecological Risk Assessment (USEPA, 1998).

Previous Assessments

Debacarb is registered for use only as a tree injection. Given this application method, it has 

historically been viewed as a “closed system” with minimal likelihood of environmental exposure

(USEPA, 2008). Therefore, there are no previous ecological risk assessments or drinking water 

exposure assessments for this chemical.

2. STRESSOR SOURCE AND DISTRIBUTION

Pesticidal Mechanism of Action

Debacarb is a fungicide belonging to the benzimidazole carbamate class of pesticides. 

Benzimidazole toxicity is based on the inhibition of the formation of spindle fibers at nuclear 

division (mitosis/meiosis), which results in the inhibition of deoxyribonucleic acid (DNA) 

replication (Davidse, 1986)

Overview of Pesticide Use and Usage

Debacarb was originally registered for use in the United States in 1982. It is used to prevent and 

treat certain fungal diseases in ornamental trees. Currently, debacarb is registered for use only as 

a tree injection application to ornamental trees. There are three active Section 3 products 

containing debacarb, i.e., Imisol® (Reg. No.7946-21, Abasol® (Reg. No. 7946-20), and Fungisol®

(Reg. No. 7946-14). All three products are co-formulated with the fungicide carbendazim (PC 

128872; CAS # 10605-21-7). According to correspondence with the registrant (J.J Mauget) in the 

1990s, debacarb and carbendazim are manufactured from benomyl (PC 099101; CAS No. 17804-

35-2), and it is technically infeasible to separate the two (letter from Donald Diamond, attorney 

representing J.J. Mauget Co., dated June 10, 1992). It should be noted however, that carbendazim 

is registered as an active ingredient in other pesticides in which debacarb is not claimed as an 

active ingredient or impurity. In addition, Imisol® is co-formulated with the insecticide 

imidacloprid (PC 129099, CAS No. 138264-41-3) and Abasol® is co-formulated with avermectin 

(PC 122804, CAS No. 71751-41-2). 

Use Rates

All three debacarb-containing products consist of 4 or 6 mL (product) capsules that are injected 

via a closed micro-injection system consisting of a feeder tube and compressible injector unit (the 
4

“Mauget System”1). The maximum number of capsules allowed per treatment is determined by 

the size of the tree as measured by the diameter at breast height (DBH). For trees with 2-10 inch 

DBH, the 4-mL capsules are prescribed, and for trees with a DBH greater than or equal to 10 

inches, the 6-mL capsules are prescribed. According to the label, treatments of trees smaller than 

2 inches DBH are not allowed. The maximum number of capsules per treatment is determined by 

dividing the DBH by two. If this results in a fraction, the label instructs the applicator to round 

down to the nearest whole number. For example, for a tree with a DBH of 16 inches the label 

allows for the injection of a total of eight 6-mL capsules per treatment. Repeat treatments are 

recommended if disease symptoms progress, but are not allowed within 3 months of the first 

application. The label does not appear to limit the number of applications per year after the required 

three month interval following the first application. Debacarb comprises 1.7% (w/w) of all three 

products (approximately 0.1 g a.i. per 6-mL capsules and 0.07 g a.i. per 4-mL capsules). Based on 

label instructions, the amount of debacarb applied to individual trees through injection of capsules 

was calculated for trees of varying DBH values (Table 1). This information is used in later sections 

of the risk assessment to estimate potential exposure and effects to organisms consuming food 

items from trees treated with debacarb

Table 1. Tree size and use parameters

Tree Diameter 

at Breast 

Height (inches)

Size of 

Capsules 

(ml)

Number of 

Capsules per 

Tree

Total Volume 

of Formulation 

per Tree (ml)

Total Grams of 

Debacarb per 

Tree per 

Application*

2 4 1 4 0.068

10 4 5 20 0.34

16 6 8 48 0.82

24 6 12 72 1.2

32 6 16 96 1.6

*Total grams ai per tree per application = total volume (ml) per tree * 0.017 (percent a.i. w/w)

Estimated Usage

The registrant estimated the number of trees treated with Fungisol® across five regions of the 

United States based on sales data and reported this information to EPA (Table 2). It should be 

noted that information on the estimated number of trees treated with the other two tree injection 

end-use products was not available at the time of this assessment. However, sales data provided to 

EPA by the registrant indicate that Fungisol® is used more than both Imisol® and Abasol®

combined (confidential data, not shown).

Table 2. Estimated number of trees treated with the product, Fungisol® in various regions 

and in total for the United States

U.S. Region

Number of trees treated with 

Fungisol® (2011)

Number of trees treated with 

Fungisol® (2012)

Northeast 3,293 3,057

Southeast 797 617

Northwest 297 384

Southwest 1,862 2,947

 

1 An example of the Mauget System can be viewed at: http://www.youtube.com/watch?v=4j1aezoAtbE (last 

accessed 06/19/2014).
5

Midwest 5,152 5,192

Total 11,401 12,197

Environmental Fate and Transport

Best-available data defining the physical, chemical, fate and transport characteristics associated 

with debacarb are summarized in Table 3. Since products containing debacarb are used to treat 

diseases such as canker, wilts, and blight, which may occur in tree trunks, limbs, and leaves, the 

compound is most likely systemic and translocated to different parts of the plant. There are 

currently no registrant-submitted data characterizing the fate and transport of debacarb in the 

environment. According to the Registration Memo, all environmental fate data requirements were 

waived during registration in 1993. Environmental fate data on the uptake and translocation of 

debacarb in plants was previously recommended (USEPA, 2008), but were not submitted. Based 

on estimations from the Estimation Program Interface Suite2(EPISuiteTM; v3.2), debacarb is 

soluble, and volatilization and bioaccumulation are not likely. Based on the Biodegradation 

Probability Program (BIOWINTM) component of EPISuiteTM, which estimates the probability for 

the rapid aerobic biodegradation of an organic chemical in the presence of mixed populations of 

environmental microorganisms, debacarb is not likely to biodegrade quickly, and ultimate 

biodegradation is expected on the order of weeks to months (Howard et al., 1992). 

Table 3. General chemical and environmental fate properties of debacarb

Chemical/Fate parameter Value Source 

Molecular Weight (g/mol) 293.33

Vapor Pressure (torr) 7.8 x 10-10 Estimated EPISuiteTM v3.2

Octanol-water Partition Coefficient (Log KOW) 1.5 Estimated EPISuiteTM v3.2

Water Solubility (mg/L; at 25 °C) 710 Estimated EPISuiteTM v3.2

Henry's Law Constant (atm-m3 mol-1) 4.8 x 10-16 Estimated EPISuiteTM v3.2

Biodegradation (mixed populations of 

environmental microorganisms)

Does not biodegrade quickly

Not readily degradable

Ultimate biodegradation: 

weeks - months 

Estimated EPISuiteTM v3.2 

(BIOWIN v4.10)

3. RECEPTORS

Ecological Effects

There are limited ecological effects data available for debacarb (Table 4). Debacarb is classified 

as slightly toxic to practically non-toxic to birds on an acute oral exposure basis (Acc. No. 

00046490, 00046491), and practically non-toxic to birds on a sub-acute dietary exposure basis

(Acc. No. 00072903). In an acute oral toxicity study with mallard ducks (Anas platyrhynchos; 

Acc. No. 00046490), some lethargy, loss of coordination, and lower limb weakness was observed 

in birds at 1,590 and 2,510 mg/kg doses. Debacarb is classified as practically non-toxic to 

 

2 USEPA. 2013. Estimation Program Interface Suite (EPI Suite). http://www.epa.gov/opptintr/exposure/pubs/episuite.htm.
6

mammals on an acute oral exposure basis (Acc. No. 244391). Acute oral mammalian toxicity data 

requirements were waived for the combination products Abasol® and Imisol®. There are no data 

on the chronic effects of debacarb on birds and mammals. Chronic studies do exist for 

carbendazim, which is also a benzimidazole fungicide with a similar structure to debacarb

(Appendix A). Therefore, data are bridged in this assessment between debacarb and carbendazim 

in cases where data are not available for the former. 

In a chronic rat study with carbendazim, decreased pup weights were noted at weaning resulting 

in a NOAEC and LOAEC of 500 and 5,000 mg/kg-diet, respectively (Acc. No. 00088333). It 

should also be noted that in an acute oral toxicity test conducted with carbendazim on rats (Acc. 

No. 256025), single doses of 1,000 mg and above resulted in adverse effects to the testes and 

caused depressed or absent spermatogenesis. In addition, when rats were administered ten doses 

of carbendazim over a two-week period at a single rate of 5,000 mg/kg-bw/day, spermatogenesis 

ceased with no evidence of recovery (Acc. No. 256025). Given the structural similarity between 

debacarb and carbendazim, implications for these potentially reproductively relevant sublethal 

effects will be discussed in the Risk Characterization section of this document.

Data on the toxicity of debacarb and its formulated products to honeybees (Apis mellifera) are not 

available. Several honeybee toxicity studies (acute contact, 850.3020; acute oral, non-guideline; 

foliage residue toxicity, 850.3030; field testing for pollinators, 850.3040) were previously 

recommended but were not submitted. It is important to note that two of the formulated products, 

Imisol® and Abasol®, contain systemic insecticides that are highly toxic to honeybees. The Imisol®

product is co-formulated with imidacloprid, an insecticide with a 48-hr acute contact LD50 value

of 0.0039 μg a.i./bee. The Abasol® product is co-formulated with avermectin, an insecticide that 

is also highly toxic to bees with a 48-hr acute contact LD50 value of 0.41 μg a.i./bee. The third 

formulated product, Fungisol®, is co-formulated with carbendazim, a fungicide that is practically 

non-toxic to bees with a 48-hr acute contact LD50 value of >50 μg a.i./bee. 

Based on a search of the public version of EPA’s ECOTOX database3on June 19, 2014, no relevant 

open literature data for terrestrial animals were identified for use in this assessment.

There are no submitted toxicity data for effects to terrestrial plants. However, based on the use 

pattern, exposure to non-target terrestrial plants is not considered likely and will not be assessed.

No valid registrant-submitted aquatic toxicity studies with either plants or animals are available 

for debacarb. No aquatic toxicity studies were recommended by EFED during the Registration 

Review Preliminary Problem Formulation (USEPA, 2008) because exposure to aquatic 

ecosystems was expected to be minimal based on the limited use pattern (ornamental tree 

injection). The uncertainties surrounding the assumption of minimal exposure are addressed in the 

Risk Description section.

 

3 http://cfpub.epa.gov/ecotox/
7

Table 4. Summary of most sensitive endpoints from submitted terrestrial toxicity studies

for debacarb

Species

(common 

name)

Taxa 

Represented

Endpoint

Mean 

Concentration

(adjusted for % 

purity)

Test Substance 

(% a.i.)

Citation

MRID

Acute Toxicity 

Classification

Rattus 

norvegicus

(Laboratory 

Rat)

Mammals

LD50

13,500 (229.5) mg

ai/kg-bw

Formulation 

(Fungisol®; 

Debacarb: 1.7; 

MBC: 0.3)

241406 Moderately 

Toxic

LD50

>5,000 (4,000) mg

a.i./kg*

80†‡ 244391 Practically nontoxic

NOAEL

500 mg/kg-diet 

25 mg/kg-bw

(MBC)

(decreased weight 

gain) 50 or 70 00088333 N/A

LOAEL

5,000 mg/kg-diet 

250 mg/kg-bw

(MBC)

Anas 

platyrhynchos

(Mallard Duck) Birds

LD50

.>2,510 (2,008) 

mg/kg 80‡ 00046490 Practically nontoxic

LD50

≥1,000 (800) 

mg/kg 80‡ 00046491 Slightly toxic

LC50

> 5,620 (4,496) 

mg/kg-diet 80‡ 00072903 Practically nontoxic

NOAEC

322 (MBC)

(Viable embryos, 

normal hatchlings, 

14 day survivors)

N/A§ 44103002

N/A

LOAEC 720 (MBC) N/A

Colinus 

virginianus

(Northern 

Bobwhite 

Quail)

LC50

> 5,620 (4,496) 

mg/kg-diet 80‡ 00046492 Practically nontoxic

NOAEC 3,600 (MBC)

N/A§ 44103001 N/A LOAEC >3,600 (MBC)

Apis mellifera

(Honey Bee)

Insect 

Pollinators LD50 >50 μg/bee (MBC) 99.3 00154695 Practically nontoxic

MBC = methyl 2- benzimidazole carbamate (carbendazim)

* Note: irreversible spermatogenic effects observed in subchronic studies

†

Information on percent a.i. was not provided in study report, but was deduced by the risk assessor by matching the 

test substance lot number (0B07) to other ecological effects studies submitted to EFED with the same lot number for 

which the percent a.i. was reported. The reported endpoint for this study was 5,000 mg/kg-bw, and was adjusted to 

4,000 mg ai/kg-bw based on the assumed 80% a.i.

‡ Based on the data review for MRID 0046491, the use of 80% debacarb active ingredient as technical is due to the 

inability to separate debacarb, carbendazim, and 2-amino-benzimidazole in the production process. Apparently, the 

technical product used for these tests was produced solely for testing purposes.

§ Endpoints based on measured MBC in diet for test with benomyl
8

Ecological Incidents

Reviews of the Ecological Incident Information System (EIIS, version 2.1), the Avian Incident 

Monitoring System (AIMS)4, and the Incident Data System (IDS) were conducted on June 19, 

2014. There were no reported ecological incidents associated with debacarb; however, as with 

other chemicals, given the limited reporting of incidents, the absence of incident reports cannot be 

construed as the absence of incidents.

4. ASSESSMENT ENDPOINTS

Based on current registered use patterns, the ecological entities that are relevant to debacarb in this 

assessment include birds, mammals, and insect pollinators that feed on translocated residues of 

debacarb in fruit, seeds, foliage, and pollen. The attributes for each of these entities may include 

growth, reproduction, and survival. A summary of the terrestrial toxicological endpoints for 

debacarb can be found in Table 3 of the Ecological Effects section. In cases where no guideline 

toxicity data were available for debacarb, data were bridged from carbendazim, a carbamate 

fungicide with a similar molecular structure to debacarb.

For aquatic organisms, no valid registrant-submitted aquatic toxicity studies with either plants or 

animals are available for debacarb and were not recommended by EFED during the Registration 

Review Preliminary Problem Formulation (USEPA, 2008) because exposure to aquatic 

ecosystems was expected to be minimal based on the limited use pattern (ornamental tree 

injection). Therefore, specific assessment endpoints for aquatic organisms are not considered in 

this assessment.

5. CONCEPTUAL MODEL

For a pesticide to pose an ecological risk, it must reach ecological receptors in biologically 

significant concentrations. An exposure pathway is the means by which a pesticide moves in the 

environment from a source to an ecological receptor. For an ecological 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.

The conceptual model for debacarb provides a written description and visual representation of the 

predicted relationships between debacarb, potential routes of exposure, and the predicted effects 

for the assessment endpoint. A conceptual model consists of two major components: risk 

hypothesis and a conceptual diagram (USEPA 1998).

Based on the use pattern and mode of action, risks to birds, mammals and terrestrial invertebrates, 

including insect pollinators, are possible. Because of the potential risk from direct effects to these

taxa, potential concerns exist for indirect effects for food, habitat, and/or pollination. This forms 

the basis of the risk hypothesis and conceptual diagram discussed below. 

In this assessment, the potential for exposure and risk to plants from debacarb is considered to be 

minimal based on the limited tree injection use pattern. The potential for exposure and risk to 

 

4http://www.abcbirds.org/abcprograms/policy/toxins/aims/aims/login.cfm?CFID=113048231&CFTOKEN=9243482
9

aquatic organisms is considered uncertain since leaves shed from trees treated with debacarb 

could potentially enter aquatic systems; however, EFED believes that potential risks to these 

systems may be reduced via use restrictions. Therefore, risks to plants and aquatic organisms are

not considered in the risk hypothesis.

Risk Hypothesis

A risk hypothesis describes the predicted relationship among the stressor, exposure, and 

assessment endpoint response along with the rationale for their selection. For debacarb, the 

following ecological risk hypothesis is being employed for this ecological risk assessment:

Based on the application method, mode of action, fate and transport, and the sensitivity of 

non-target terrestrial species, debacarb has the potential to reduce survival, reproduction, 

and/or growth in non-target terrestrial animals including birds, mammals, and 

invertebrates, including insect pollinators, when used in accordance with the current label. 

These non-target organisms include federally listed threatened and endangered species as 

well as non-listed species.

Conceptual Diagram

Given the specificity of the tree injection use pattern, the only viable transport mechanism consists 

of translocation/uptake to various parts of treated trees, including foliage, fruit, seeds, and pollen. 

The transport mechanism (i.e., source) is depicted in the conceptual model below (Figure 1) along 

with the receptors of concern and the potential attribute changes in the receptors due to exposures 

of debacarb. The conceptual model also depicts the potential for debacarb residues in leaves, 

fruits, and seeds to drop into adjacent water bodies; however, exposures to aquatic receptors via 

this pathway are expected to be minimal given the limited tree injection use pattern. However, the 

uncertainty surrounding this assumption is discussed in the Risk Description.
10

Figure 1. Conceptual model for debacarb effects on terrestrial organisms. Dotted lines 

indicate exposure pathways that have a low likelihood of contributing to ecological risk. 

Stressor

Source

Receptors

Attribute

Change

Debacarb applied to use site (tree injection)

Direct 

application

Individual organisms

Reduced survival

Reduced growth

Reduced reproduction

Terrestrial food items (various 

parts of tree, including fruit, 

seeds, foliage, nectar, pollen)

Mammals

Exposure

Media

Direct Contact/ 

Ingestion

Ingestion Ingestion

Translocation/uptake

Terrestrial Birds 

insects

Aquatic 

Organisms

Shedding 

leaves
11

6. ANALYSIS

In order to address the risk hypothesis, the potential for adverse effects to non-target organisms is 

estimated. The use, environmental fate, and ecological effects of debacarb are characterized and 

integrated to assess risk by using a risk quotient (ratio of exposure concentration to effects 

concentration) approach when possible. When a risk quotient approach is not possible, risks are 

assessed qualitatively.

Stressors of Concern

Due to the limited use pattern, there are no environmental fate data for debacarb. The route of 

exposure to terrestrial organisms is through uptake and translocation of debacarb to various parts 

of treated trees, including foliage, fruit, seeds, nectar, and pollen which can in turn be used as food 

items by other organisms. There are no data on the rate of translocation or decay of debacarb in 

ornamental trees nor have transformation products been identified. Biodegradation modeling 

suggests that debacarb is not likely to biodegrade quickly, and ultimate biodegradation is expected 

on the order of week to months. As such, the focus of this assessment is expected to be the parent, 

debacarb, with the assumption that it does not degrade appreciably in trees. Additionally, 

formulated products containing avermectin (Abasol®) and imidicloprid (Imisol®) will be 

considered with respect to potential adverse effects on insect pollinators.

Measures of Exposure 

The route of exposure to terrestrial organisms is through uptake and translocation of debacarb to 

foliage/fruit/seeds/nectar/pollen which can be used as food items. Biodegradation modeling 

suggests that debacarb is not likely to biodegrade quickly, and ultimate biodegradation is expected 

on the order of week to months. No environmental fate data pertaining to the amount and rate of 

translocation and/or decay of debacarb in trees following application are available to facilitate 

estimation of potential residues in foliage/fruit/seeds/nectar/pollen which can be used as food items 

for terrestrial organisms. Therefore, as a conservative screening approach, it will be assumed that 

the total amount of debacarb applied to the target tree will be evenly distributed throughout the 

foliage (i.e., leaves), and that terrestrial animals feed exclusively on foliage (a surrogate for other 

non-woody food items such as fruit) from trees treated with debacarb.

For estimating residues of debacarb in foliage, both hardwood (typically deciduous) and softwood 

(typically evergreen) trees are considered, since debacarb may be applied to both types of trees. 

Leaf biomass (dry weight) for hardwoods and softwoods were estimated using equations described 

in Jenkins et al. 2004 and parameter values from Sollins (1973), as follows:

Estimate biomass of foliage for hardwood and softwood trees:

General hardwood equation for dry weight (Sollins et al., 1973)

ln leaf biomass (kg) = -3.862 + 1.74*(ln(dbh [in cm]))

General softwood equation for dry weight (Sollins et al., 1973):

ln leaf biomass (kg) = -2.907 + 1.674*(ln(dbh [in cm]))
12

Reverse natural log (ln) of leaf biomass:

Leaf biomass= eln leaf biomass

The correction for bias when converting from ln to arithmetic units = 1.34 (Sollins et al., 

1973):

Leaf biomass (corrected) = (uncorrected weight)*1.34

For leaves, 85 percent (mean) of the wet weight is water (USEPA, 1993); therefore, the 

general equation to convert leaf dry weight into wet weight is:

Leaf wet weight = (100% total leaf weight) *(kg of leaf dry weight)/(% leaf dry weight) 

Table 5 summarizes the estimated dry and wet leaf biomasses for trees of varying DBH values.

Table 5. Summary of Leaf Biomass for Different Tree Diameters

Tree Diameter at 

Breast Height 

(inches)

Hardwood Trees Softwood Trees

Dry Weight 

Leaf Biomass 

(kg)

Wet Weight 

Leaf Biomass 

(kg)

Dry Weight 

Leaf Biomass 

(kg)

Wet Weight Leaf 

Biomass (kg)

2 0.48 3.18 1.11 7.42

10 7.84 52.26 16.46 109.70

16 17.76 118.40 36.14 240.94

24 35.96 239.74 71.25 474.99

32 59.32 395.49 115.32 768.83

For simplicity, it is conservatively assumed that the entire application of debacarb will accumulate 

in the leaves (a surrogate for other non-woody food items such as seeds) of the tree. To determine 

the dietary concentration (i.e., EEC) of debacarb in the leaves of hardwoods and softwoods, the 

total debacarb application amount per tree is divided by the total leaf biomass (based on wet 

weight) of the tree. Results are presented in Table 6. For example, for a hardwood tree of 2 inch 

DBH, 68 mg a.i./tree (from Table 1) is applied to the tree and is divided by 3.18 kg foliage wet 

weight (from Table 5), resulting in a concentration of 21.4 mg a.i./kg-leaves. The resulting EECs 

are used as an estimate of the dietary concentration of debacarb in bird and mammal food items.

Table 6. Summary of EECs (unadjusted) for Debacarb Residues in Tree Foliage for 

Different Tree Diameters

Tree Diameter at 

Breast Height 

(inches)

Concentration (mg a.i./kg-leaves)

Hardwood Trees Softwood Trees

2 21.41 9.17

10 6.51 3.10

16 6.93 3.40

24 5.01 2.53

32 4.05 2.08

In order to obtain dose-based exposure estimates for birds and mammals, the dietary EECs must 

be adjusted for mammal and bird body weights (Table 7 and 8). EFED’s terrestrial exposure 
13

model, T-REX

5

, uses three size classes for mammals: 15, 35, and 1000 g, and three size classes 

for birds: 20, 100, and 1000 g. According to the T-REX User’s Manual6, a 15-g mammal consumes 

95 percent of its body weight daily, a 35-g mammal consumes 66 percent of its body weight daily, 

and a 1000-g mammal consumes 15 percent of its body weight daily. A 20-g bird consumes 114

percent of its body weight daily, a 100-g bird consumes 65 percent of its body weight daily, and a 

1000 g bird consumes 29 percent of its body weight daily.

Consequently, the general equation for determining the debacarb dose per day is:

EEC mg a.i./kg-bw = (dietary concentration mg a.i./kg-diet)*(body weight consumption 

kg-diet/kg-bw).

For example, for a 15-g mammal feeding on a 2 DBH hardwood tree, EEC = 21.4 mg a.i./kgdiet)*(0.95 kg-diet/kg-bw) = 20.34 mg a.i./kg-bw.

The estimated exposure values presented in Tables 7 and 8 will be combined with available 

toxicity data for mammals and birds for RQ calculations in this assessment.

Table 7. Summary of Mammalian Body Weight-Adjusted EECs for Different Tree 

Diameters

Tree Diameter 

at Breast Height 

(inches)

Hardwood Trees Softwood Trees

Dietary 

Concentrations

(mg/kg-diet)

Dose-Based 

Concentrations

(mg/kg-bw)

Dietary 

Concentrations

(mg/kg-diet)

Dose-Based Concentrations

(mg/kg-bw)

15g 35g 1000g 15g 35g 1000g

2 21.41 20.34 14.13 3.21 9.17 8.71 6.05 1.38

10 6.51 6.18 4.29 0.98 3.10 2.94 2.05 0.46

16 6.93 6.58 4.57 1.04 3.40 3.23 2.25 0.51

24 5.01 4.76 3.30 0.75 2.53 2.40 1.67 0.38

32 4.05 3.84 2.67 0.61 2.08 1.98 1.37 0.31

Table 8. Summary of Avian Body Weight-Adjusted EECs for Different Tree Diameters

Tree Diameter 

at Breast Height 

(inches)

Hardwood Trees Softwood Trees

Dietary 

Concentrations

(mg/kg-diet)

Dose-Based 

Concentrations

(mg/kg-bw)

Dietary 

Concentrations

(mg/kg-diet)

Dose-Based Concentrations

(mg/kg-bw)

20g 100g 1000g 20g 100g 1000g

2 21.41 24.40 13.91 6.21 9.17 10.45 5.96 2.66

10 6.51 7.42 4.23 1.89 3.10 3.53 2.01 0.90

16 6.93 7.90 4.50 2.01 3.40 3.88 2.21 0.99

24 5.01 5.71 3.25 1.45 2.53 2.88 1.64 0.73

32 4.05 4.61 2.63 1.17 2.08 2.37 1.35 0.60

Measures of Effect

Where available, sublethal effects observed in both registrant-submitted and open literature studies 

are evaluated qualitatively. In the available debacarb toxicity studies, such effects include 

 

5 http://www.epa.gov/oppefed1/models/terrestrial/

6 http://www.epa.gov/oppefed1/models/terrestrial/trex/t_rex_user_guide.htm
14

lethargy, loss of coordination, lower limb weakness, and slight reduction in body weight gain (not 

statistically evaluated), as well as decreased or absent spermatogenesis (based on carbendazim).

Quantitative assessments of risks, though, are limited to those endpoints that can be directly linked 

to the Agency’s assessment endpoints of impaired survival, growth and reproduction.

The assessment of risk for direct effects to non-target organisms makes the assumption that in the 

absence of data to the contrary, toxicity of debacarb to birds is similar to that for terrestrial-phase 

amphibians and reptiles. However, the appropriateness of birds as surrogates for these other groups 

is discussed in the Risk Description. The acute measures of effect used for animals in this 

screening-level assessment are the acute LD50 and LC50. Endpoints for chronic measures of 

exposure for listed and non-listed animals are the NOAEL and/or NOAEC. 

Integration of Exposure and Effects

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

determine the potential ecological risk from the use of debacarb for tree injections, and the 

likelihood of direct and/or indirect effects to non-target organisms in terrestrial habitats. For 

terrestrial organisms, the exposure and toxicity data are integrated in order to evaluate the 

likelihood of adverse ecological effects to non-target species from exposure, i.e, risk. For the 

assessment of debacarb exposure and potential risks associated with the tree injection use, the risk 

quotient (RQ) method is used to compare exposure and measured toxicity values. EECs are 

divided by the acute and chronic toxicity values (if available). The resulting RQ values are then 

compared to the Agency’s LOC values (USEPA, 2004) (see Table 9). These criteria are used, in 

addition to other available data (e.g., incident data), to indicate when debacarb’s uses, as directed 

on the label, have the potential to cause adverse direct or indirect effects to non-target organisms.

TABLE 9. Agency Levels of Concern (LOC) for Birds and Mammals

Risk Description RQ

Acute

Potential for acute risk to non-target organisms 

which may warrant regulatory action in addition 

to restricted use classification

acute RQ > 0.5

Acute Listed 

Species

Listed species may be potentially affected by 

use

acute RQ > 0.1

Chronic

Potential for chronic risk may warrant 

regulatory action, listed species may potentially 

be affected through chronic exposure

chronic RQ > 1
15

7. RISK CHARACTERIZATION

Risk Estimation

Mammals

The only available mammalian acute oral toxicity study for debacarb technical is non-definitive 

and resulted in an LD50 >4,000 mg a.i./kg-bw. In addition, an acute oral mammalian study is 

available for the Fungisol

® end-product (LD50 = 229.5 mg a.i./kg-bw). For screening-level 

assessment purposes, RQs were calculated based on the LD50 for Fungisol® (229.5 mg a.i./kg-bw) 

since it is more sensitive than the technical. Since chronic toxicity data were not available for 

debacarb, chronic RQs for debacarb were calculated based on a NOAEC of 500 mg/kg-diet (35 

mg/kg-bw), which was the lowest rat two-generation toxicity endpoint value for carbendazim. In 

order to calculate acute and chronic dose-based RQs for mammals, LD50 and NOAEC values were 

corrected using a scaling factor of 1.15 (from Mineau et al., 1996) as implemented in T-REX7, 

resulting in LD50 values of 504, 408, and 177 mg a.i./kg-bw for 15-, 35-, and 1000-g sized

mammals, respectively, for the Fungisol® end-product, and NOAEC values of 55, 44, and 19 mg

a.i./kg-bw.

Acute dose-based screening-level RQs for Fungisol® are presented in Table 10 and are below the 

acute risk LOC of 0.1 for listed mammals. Chronic RQs are presented in Table 11 and do not 

exceed the chronic risk LOC of 1 for mammals.

Table 10. Acute Risk Estimates for Mammals

Tree Diameter 

at Breast Height 

(inches)

Acute Dose-Based RQs

Hardwood Trees Softwood Trees

15g 35g 1000g 15g 35g 1000g

2 0.04 0.03 0.02 0.02 0.01 0.01

10 0.01 0.01 0.01 0.01 0.01 <0.01

16 0.01 0.01 0.01 0.01 0.01 <0.01

24 0.01 0.01 <0.01 <0.01 <0.01 <0.01

32 0.01 0.01 <0.01 <0.01 <0.01 <0.01

Table 11. Chronic Risk Estimates for Mammals

Tree Diameter

at Breast Height 

(inches)

Chronic Dose-Based RQs Chronic Dietary-Based RQs

Hardwood Trees Softwood Trees Hardwood 

Trees

Softwood 

Trees 15g 35g 1000g 15g 35g 1000g

2 0.37 0.32 0.17 0.16 0.14 0.07 0.04 0.02

10 0.11 0.10 0.05 0.05 0.05 0.02 0.01 0.01

16 0.12 0.10 0.05 0.06 0.05 0.03 0.01 0.01

24 0.09 0.07 0.04 0.04 0.04 0.02 0.01 0.01

32 0.07 0.06 0.03 0.04 0.03 0.02 0.01 <0.01

 

7 http://www.epa.gov/oppefed1/models/terrestrial/
16

Birds

The only available avian acute oral toxicity study for debacarb is non-definitive and resulted in an 

LD50 >800 mg a.i./kg-bw. Both available avian subacute dietary toxicity studies for debacarb are 

also non-definitive and resulted in an LC50 >4,496 mg a.i./kg-diet for bobwhite quail (Colinus 

virginianus) and mallard duck (Anas platyrhynchos). Since RQs cannot be calculated based on 

non-definitive endpoints, for screening-level assessment purposes, acute dose- and dietary-based 

EECs were compared to the highest doses and concentrations tested in available acute oral (800

mg a.i./kg-bw) and acute dietary (4,496 mg a.i./kg-diet) studies, respectively. However, in order 

to compare avian acute oral toxicity data to acute dose-based EECs, the highest concentration 

tested (800 mg a.i./kg-bw) was first corrected for food consumption rate using a scaling factor of 

1.15, resulting in values of 415, 529, and 747 mg/kg-bw for 20-, 100-, and 1000-g sized birds, 

respectively. To calculate chronic RQ values, the lowest toxicity value for carbendazim 

(NOAEC=322 mg/kg-diet, mallard duck) was used.

Acute dose- and dietary-based EECs are at least 10 times lower than the highest doses and 

concentrations tested in available acute oral and acute dietary studies, respectively, for birds. 

Therefore, there do not appear to be acute risks of concern to listed or non-listed birds. In 

addition, no chronic RQs exceed the chronic LOC of 1 for birds (Table 12). 

Table 12. Chronic Risk Estimates for Birds

Tree Diameter 

at Breast Height 

(inches)

Chronic Dietary-Based RQs

Hardwood 

Trees

Softwood 

Trees

2 0.07 0.03

10 0.02 0.01

16 0.02 0.01

24 0.02 0.01

32 0.01 0.01

Insect Pollinators

RQs were not calculated for insect pollinators since no definitive toxicity data for honeybees are 

available for debacarb or carbendazim. Potential risks to insect pollinators are further discussed in 

the Risk Description section.

Risk Description

Based on information provided by the registrant, the number of trees treated with products 

containing debacarb in the U.S. is estimated to be in the thousands to tens of thousands (Table 2). 

Since the total number of trees in the U.S. has been estimated in the hundreds of billions8, the 

proportion of trees treated with debacarb nationwide is extremely small. Therefore, the potential 

for exposure of non-target organisms to debacarb is expected to be low. However, it is possible 

that a large number of trees may be treated in a given area at a given time, which could potentially 

lead to increased exposure. This uncertainty was considered to be greater for terrestrial animals

 

8 http://www.fia.fs.fed.us/tools-data/maps/2007/descr/livetredbh1.asp
17

because they could feed directly on contaminated food items, and was dealt with quantitatively in 

this assessment by assuming that birds and mammals forage exclusively on trees treated with 

debacarb. For aquatic organisms, this uncertainty is considered qualitatively along with other lines 

of evidence indicating low potential for exposure to aquatic systems.

Terrestrial Organisms

A conservative screening-level risk analysis was performed in this assessment in which terrestrial 

vertebrates were assumed to feed 100 percent of their diet on the foliage of trees treated with 

debacarb. As mentioned above, given the low number of trees estimated to have been treated with 

Fungisol® in 2011 and 2012, this is a very conservative assumption (Table 2). Further 

conservatism was built into this analysis in the sense that the entire tree injection of debacarb was 

assumed to migrate to the tree foliage, which was used as a surrogate for dietary items upon which 

birds and mammals feed (i.e., fruits, nuts, seeds). The latter assumption was made because 

environmental fate data on the uptake and translocation of debacarb in plants was requested but 

not submitted. However, given that the target pests indicated on the product labels (e.g., various 

types of plant canker) can also affect the bark and other woody or stem portions of the plant, it is 

unlikely that debacarb moves entirely into the foliage or else in would not be effective. Based on 

this conservative screening-level analysis, no risks of concern were identified for mammals or 

birds, including reptiles and terrestrial-phase amphibians for which birds serve as surrogates. 

Although significant acute sublethal effects on spermatogenesis were observed in rats at single 

oral doses of carbendazim starting at 1,000 mg/kg-bw, conservative exposure estimates for 

residues in food items are well below the doses at which this effect was observed. Risk conclusions 

for birds and mammals were based partly on chronic toxicity data from carbendazim, which was 

used to bridge data since it has a similar molecular structure to debacarb; therefore, the absence of 

chronic toxicity data for debacarb is considered an uncertainty.

Since debacarb is systemic, there is potential for exposure to insect pollinators from residues 

translocated to pollen and nectar of treated trees. No definitive toxicity data are available for 

honeybees exposed to debacarb. Therefore, RQs could not be calculated to evaluate risk to insect 

pollinators in this assessment. While there is acute toxicity data for carbendazim indicating that 

the compound is practically non-toxic to honeybees on a contact exposure basis (Table 3), this 

type of data does not account for potential toxicity through the oral exposure route, i.e., ingestion 

of residues through pollen and nectar. Therefore, the absence of toxicity data for debacarb to 

honeybees via the oral exposure route is considered an uncertainty in this assessment. While a 

relatively low number of trees are estimated to be treated with debacarb each year across the U.S., 

the magnitude of this uncertainty, in part, depends on whether groups of trees are treated in close 

proximity to each other, at the same time, and during parts of the year when residues are more 

likely to be translocated to pollen or nectar, all of which would be more likely to result in increased 

exposure. In addition, based on biodegradation modeling, debacarb is likely to be persistent, 

increasing the potential window of exposure. It is also important to note that two of the formulated 

products, Imisol® and Abasol®, contain systemic insecticides that are highly toxic to honeybees. 

The Imisol® product is co-formulated with imidacloprid, an insecticide with an acute contact LD50

value of 0.0039 μg/bee. The Abasol® product is co-formulated with avermectin, an insecticide 

that is also highly toxic to bees with an acute contact LD50 value of 0.41 μg/bee. The current label 

for Abasol® indicates that it should only be used as a post-bloom application, while the labels for 
18

Imisol® and Fungisol® do not have any application restrictions relative to bloom. Based on these 

uncertainties, potential risks of concern to honeybees cannot be precluded. 

Potential risks of concern to other terrestrial invertebrate species also cannot be precluded since 

some species may consume various edible plant parts containing translocated residues (e.g., leaves, 

fruit) and since there are no available toxicity data for debacarb for any terrestrial invertebrate

species

Aquatic Organisms

The potential for exposure to aquatic organisms from residues of debacarb in leaves, fruits, and 

seeds of treated trees that fall into adjacent water bodies was previously acknowledged, but was 

not considered to be a significant route of exposure in the Preliminary Problem Formulation for 

Registration Review (USEPA, 2008). Therefore, environmental fate and aquatic toxicity studies 

for debacarb were not previously recommended to evaluate exposure and effects to aquatic 

organisms for the tree injection use.

The major uncertainty concerning the potential for debacarb to reach aquatic environments is that 

the chemical could migrate to portions of treated trees (e.g., leaves) that may be subsequently shed; 

if treated trees are located in close proximity to aquatic systems, the shed material could end up in 

water bodies and result in exposure of aquatic organisms to debacarb.

There are several reasons why debacarb is not expected to enter water bodies in sufficient amounts 

that would lead to risks of concern. First, the low number of trees treated per year nationwide

suggests that the amount of loading of foliage containing debacarb residues into any specific 

aquatic system is likely to be small. An exception would be if many trees were treated in the same 

location at around the same time of year. Second, it is uncertain whether a large proportion of the 

debacarb residues would migrate to the foliage, where it would be available to be transported to 

aquatic system via shedding of leaves. The target pests indicated on debacarb product labels (e.g.,

various types of plant canker) appear also to affect the bark or other woody or stem portions of the 

plant; therefore, in order to be effective, a portion of debacarb residues would have to reside in 

these portions of the plant, not in the foliage. Finally, substantial amounts of foliage containing 

debacarb are only likely to end up in a water body if the treated trees are in close proximity to

water bodies. Therefore, EFED believes that potential risks to aquatic organisms may be reduced 

via use restrictions.

8. ENDANGERED SPECIES ASSESSMENT

Since direct adverse effects are not expected for birds, reptiles, terrestrial-phase amphibians, 

mammals, or terrestrial plants, the EPA makes a No Effects (NE) determination for all Federallylisted species within these groups and a No Habitat Modification determination for all designated 

critical habitats associated with these species for the currently registered uses of debacarb. Risks 

to listed aquatic organisms from the use of debacarb may potentially be mitigated via label 

amendment, but effects and habitat modification determinations cannot be made at this time. Risks 

of concern cannot be precluded for listed terrestrial invertebrates, so effects and habitat 

modification determinations also cannot be made at this time.
19

9. ENDOCRINE DISRUPTOR SCREENING PROGRAM

As required by FIFRA and FFDCA, EPA reviews numerous studies to assess potential adverse 

outcomes from exposure to chemicals. Collectively, these studies include acute, subchronic and 

chronic toxicity, including assessments of carcinogenicity, neurotoxicity, developmental,

reproductive, and general or systemic toxicity. These studies include endpoints which may be 

susceptible to endocrine influence, including effects on endocrine target organ histopathology, 

organ weights, estrus cyclicity, sexual maturation, fertility, pregnancy rates, reproductive loss, and 

sex ratios in offspring. For ecological hazard assessments, EPA evaluates acute tests and chronic 

studies that assess growth, developmental and reproductive effects in different taxonomic groups. 

As part of its most recent registration decision for debacarb, EPA reviewed these data and selected 

the most sensitive endpoints for relevant risk assessment scenarios from the existing hazard 

database. However, as required by FFDCA section 408(p), debacarb is subject to the endocrine 

screening part of the Endocrine Disruptor Screening Program (EDSP). 

EPA has developed the EDSP to determine whether certain substances (including pesticide active 

and other ingredients) may have an effect in humans or wildlife similar to an effect produced by a 

“naturally occurring estrogen, or other such endocrine effects as the Administrator may designate.” 

The EDSP employs a two-tiered approach to making the statutorily required determinations. Tier 

1 consists of a battery of 11 screening assays to identify the potential of a chemical substance to 

interact with the estrogen, androgen, or thyroid (E, A, or T) hormonal systems. Chemicals that go 

through Tier 1 screening and are found to have the potential to interact with E, A, or T hormonal 

systems will proceed to the next stage of the EDSP where EPA will determine which, if any, of 

the Tier 2 tests are necessary based on the available data. Tier 2 testing is designed to identify any 

adverse endocrine-related effects caused by the substance, and establish a dose-response 

relationship between the dose and the E, A, or T effect. 

Under FFDCA section 408(p), the Agency must screen all pesticide chemicals. Between October 

2009 and February 2010, EPA issued test orders/data call-ins for the first group of 67 chemicals, 

which contains 58 pesticide active ingredients and 9 inert ingredients. A second list of chemicals 

identified for EDSP screening was published on June 14, 20139and includes some pesticides 

scheduled for registration review and chemicals found in water. Neither of these lists should be 

construed as a list of known or likely endocrine disruptors. 

For further information on the status of the EDSP, the policies and procedures, the lists of 

chemicals, future lists, the test guidelines and the Tier 1 screening battery, please visit our 

website.10

10. REFERENCES

Davidse, L.C. 1986. Benzimidazole fungicide mechanism of action and biological impact. Ann. 

Rev. Phytopathology 24: 43-65.

 

9 See http://www.regulations.gov/#!documentDetail;D=EPA-HQ-OPPT-2009-0477-0074 for the final second list of 

chemicals.

10 http://www.epa.gov/endo/
20

Jenkins, J., D. Chojinacky, L. Heath, and R. Birdsey. 2003. Comprehensive database of diameterbased biomass regressions for North American tree species. General Technical Report NE319, Forest Service, United States Department of Agriculture. 

Howard, P.H., Boethling, R.S., Stiteler, W.M., Meylan, W.M., Hueber, A.E., Beauman, J.A., and 

M.E. Larosche. 1992. Predictive model for aerobic biodegradability developed from a file 

of evaluated biodegradation data. Environ. Toxicol. Chem. 11: 593-603.

Sollins, P., D. E. Reichle, J. S. Olson. 1973. Organic matter budget and model for a southern 

Appalachian Lirodendron forest. Publication EDFB-IBP-73-2. Oak Ridge, TN: Oak Ridge 

National Laboratory.

USEPA. 1998. Guidelines for Ecological Risk Assessment. Risk Assessment Forum, Office of 

Research and Development, Washington, D.C. EPA/630/R-95/002F. April 1998. 

http://cfpub.epa.gov/ncea/cfm/recordisplay.cfm?deid=30759 

USEPA. 1993. Wildlife Exposure Handbook, Volume I of II. Office of Research and 

Development, Washington, DC. EPA/600/R-93/187a.

USEPA. 2004. Overview of the Ecological Risk Assessment Process in the Office of Pesticide 

Programs. U.S. Environmental Protection Agency, Office of Prevention, Pesticides and Toxic 

Substances, Office of Pesticide Programs, Washington DC. January 23, 2004.

USEPA, 2008. Registration Review: Preliminary Problem Formulation for Ecological Risk, 

Environmental Fate, Endangered Species, and Drinking Water Assessments for Debacarb (2-

EEEBC). DP Barcode 357028.
21

Appendix A. Physicochemical Comparison of Debacarb and Carbendazim

Property Debacarb Carbendazim*

Chemical 

Structure

Chemical Group Benzimidazole Benzimidazole

CAS Number 17804-35-2

Molecular Weight

(g/mol) 293.33 191.18 g Mole-1

Log KOW 1.5 (estimated) 1.52

Water solubility at 

25○C (mg L-1)

710 (estimated) 8

Vapor pressure 

(Torr) 7.8 x 10-10 (estimated) 7.5 x 10-10

Henry’s Law 

Constant (atm cu 

m3 mole-1)

4.8 x 10-16 (estimated) 2.4 x 10-11

* Data for carbendazim is derived from Table 3 of “USEPA 2014. Preliminary Problem Formulation for the 

Environmental Fate, Ecological Risk, Endangered Species, and Human Health Drinking Water Exposure 

Assessments in Support of the Registration Review of Thiophanate Methyl and Carbendazim (D413077 and 

D413078)”