Page 2 of 22

C. Lewis, DP219775, 10/30/95). Based on the current use profile, exposures can be 

expected to occur via the dietary (food and drinking water) and occupational (handler and 

post-application) routes for prosulfuron.

The toxicology database for prosulfuron is considered substantially complete for the 

purposes of registration review risk assessment. An immunotoxicity study is the only 

remaining data requirement. 

Prosulfuron has low toxicity by the oral, dermal, and inhalation routes of exposure and is 

not considered an eye or skin irritant. Acceptable Developmental, reproductive and 

neurotoxicity studies are available for prosulfuron. There was no evidence from the 

developmental and reproductive studies of increased susceptibility in rat or rabbit fetuses. 

Evidence of neurotoxicity was observed in gavage but not dietary dosing studies with 

prosulfuron. The neurological effects seen in the acute neurotoxicity study were 

consistent with transient neurotoxicity affecting primary sensorimotor and gait functions. 

There was also evidence of neurotoxicity and neuropathology in a developmental rangefinding study in rabbits at all doses tested. Also in the rabbit developmental rangefinding study ataxia, hypoactivity, and neuropathology were observed. However, the 90-

day neurotoxicity study in rats did not result in any significant neurotoxicity; other 

dietary studies in the rat, mouse and dog also did not show evidence of neurotoxicity. 

Upon receipt of the required immunotoxicity study, HED will reevaluate the points of 

departure and uncertainty factors for the dietary and occupational exposure assessments.

Under the old cancer guideline classification system, the Agency classified prosulfuron as 

a Group D Chemical; ―Not Classifiable as to Human Carcinogenicity‖ (1995). The 

Agency has since reaffirmed this classification in subsequesnt evaluations. In accordance 

with the 2005 Guidelines for Carcinogen Risk Assessment, prosulfuron is classified as 

―Not Likely to Be Carcinogenic to Humans” based on the lack of evidence of 

carcinogenicity in mice and rats and no concern for mutagenicity. 

The existing residue chemistry database for prosulfuron is adequate for risk assessment 

purposes. The qualitative nature of the residue(s) of prosulfuron in plants and animals 

has been adequately identified/characterized and is understood and adequate enforcement 

analytical methods are available. The current tolerance expression as listed in the 40 

CFR§180.481 has not been updated to reflect current HED policies and thus will need to 

be revised during the registration review process.

The dietary exposure database is also adequate to support the existing registrations. In 

the last dietary assessment, the chronic and acute dietary exposure for food and water was 

not greater than 1% of the cPAD or the aPAD for all population groups. A cancer dietary 

risk assessment is not required for prosulfuron.

There are currently no residential uses for prosulfuron; therefore, a residential risk 

assessment was not required.

Updated aggregate exposure and risk assessments may be required if the toxicological 

endpoints change or other new data are received by the Agency which impact dietary 
Page 3 of 22

exposure estimates. The assessments would include combining food and drinking water 

only since there are no registered residential uses of prosulfuron.

The occupational exposure database is adequate to support the registration review process 

for prosulfuron. In the 2005 exposure assessments, all of the non-cancer occupational 

handler risk estimates were below the Agency’s level of concern. No new occupational 

handler or post-application worker studies are needed at this time. Revised occupational 

handler assessments would be based upon revisions to the Agency’s scenario-specific 

surrogate handler exposure data (http://www.epa.gov/pesticides/science/handlerexposure-table.pdf). 

Introduction

Prosulfuron is a selective herbicide used for weed control in several crops. HED has 

reviewed the most recent exposure and risk assessments for prosulfuron, as well as 

toxicity data, exposure and usage databases, and the latest Agency science policy and risk 

assessment methodologies to determine if sufficient data are available and if updates are 

needed to support registration review. Additionally, the team conducted a screeninglevel literature search for any information that would aid in assessing human health risks 

to prosulfuron.

Chemical Identity

Prosulfuron, 1-(4-methoxy-6-methyl-1,3,5-triazin-2-yl)-3-[2-(3,3,3-trifluoropropyl)-

Phenyl sulfonyl]-urea, is a selective herbicide used for weed control in or on field corn 

(grown for grain, silage, or seed), popcorn, grain sorghum (milo), wheat, barley, rye oats, 

triticale, proso millet, and following small grain harvest. It is used for ground or aerial 

spray treatment. In addition, pre-emergence applications may be made in some areas for 

broadleaf weed control in sorghum. 

The nomenclature and physicochemical properties of prosulfuron are presented in Tables 

1 and 2.

Hazard Identification/Toxicology

The toxicology database for prosulfuron is nearly complete at the present time with the 

exception of an immunotoxicity study (Table 3). The toxicity profile of prosulfuron 

developed from acute, subchronic, chronic and other studies is presented in Tables 4 and

5.

Prosulfuron has low toxicity by the oral, dermal, and inhalation routes of exposure and is 

not considered an eye or skin irritant. Chronic and subchronic studies with prosulfuron 

indicated possible treatment-related effects. The most prevalent effect observed across 

studies was on body weight. In a subchronic oral toxicity study in rats, there were 

reductions in mean body weights. Subchronic oral toxicity study in dogs showed that 

exposure to prosulfuron resulted in not only decreased body weights but also 

hematological parameters and hepatic toxicity. Similar findings were also found in the 1-
Page 4 of 22

year chronic feeding study in dogs and the 2-year rat chronic toxicity/carcinogenicity 

study. 

HED classified prosulfuron as a Group D Chemical; ―Not Classifiable as to Human 

Carcinogenicity‖, under the old cancer guideline classification system

(1995) HED has since reaffirmed this classification in subsequent evaluations. This 

classification was based on the lack of evidence of carcinogenicity in male or female 

mice at the limit dose and equivocal evidence of carcinogenicity in female rats. In female

rats, there was suggestive evidence of a possible treatment-related increase in the 

incidence of adenocarcinomas of the mammary glands at the mid dose but not at the high 

dose. This lack of dose-response (i.e. the relatively limited response in the high dose 

group and a more pronounced response in the middle-dose group) along with the lack of 

evidence of carcinogenicity in mice and the lack of evidence for in vivo or vitro

mutagenicity lowered the concern for the carcinogenic potential of prosulfuron. Thus, in 

accordance with the 2005 Guidelines for Carcinogen Risk Assessment, prosulfuron is 

classified as ―Not Likely to Be Carcinogenic to Humans” based on the lack of evidence 

of carcinogenicity in mice and rats and no concern for mutagenicity. 

In the first of two rabbit developmental studies, there were no signs of maternal or 

developmental toxicity. However, in the rabbit range-finding study that used higher 

doses, not only were there neurotoxicity effects but there were also decreased body 

weights and increased skeletal malformations. The rat and the second rabbit (tested using 

higher doses than the first) developmental studies showed dose-related increases in small 

fetuses and skeletal effects. In the reproductive study, decreases in body weights were 

noted for both the adults of the P0 and P1 generations and for the F1 and F2 offspring as 

pups. However, there was no evidence from the developmental and reproductive studies 

of increased susceptibility in rat or rabbit fetuses.

Metabolism studies were conducted for prosulfuron in rats. In both of the rat studies, 

approximately 90% of the administered dose was excreted during the first 48 hours. At 

higher doses a greater proportion of the administered dose was excreted in the feces 

compared to urine. Females usually excreted more of the dose in the urine than males in 

both instances. The major routes of metabolism occurred via hydroxylation at side chains 

and phenyl ring positions, and O-demethylation of the triazyl methoxy group or Odemethylation of the methoxy group, and hydroxylation of the triazinyl methyl group. 

Minor routes of metabolism included unsaturation of the trifluoropropyl side chain, 

hydrolysis of the phenyl-sulfonylurea link, and oxidative/hydrolytic cleavage of the 

triazine ring system. 

HED has fully evaluated the toxicity database of prosulfuron with respect to the potential 

for special sensitivity of infants and children. HED concludes that there is no concern for 

pre- and postnatal susceptibility for infants and children. The FQPA safety factor has 

been reduced to 1X because (1) the lack of evidence of increased pre- and/or postnatal

sensitivity; (2) the evidence of neurotoxicity found only after gavage dosing at dose 

levels in excess of those where systemic toxicity occurred and at a dose at least 15-fold 

higher than the NOAELs selected for risk assessment; (3) no neurotoxicity was observed 

in the subchronic neurotoxicity study in rats; (4) the neuropathology observed in pregnant 
Page 5 of 22

rabbits only occurred at dose levels where mortality and abortions were observed; and (5) 

the lesions in the spinal cord and sciatic nerve showed no dose-response.

Acceptable acute and subchronic neurotoxicity studies are available for prosulfuron. 

Evidence of neurotoxicity was observed in gavage but not dietary dosing studies with 

prosulfuron. Staggered gait, lacrimation, and hyposensitivity to touch and sound were 

seen in an acute oral study in rats. In addition, evidence of neurotoxicity (transiently 

decreased motor activity, ataxia and abnormal gait, impaired righting reflex, decreased 

body temperature) was observed in the acute neurotoxicity acute study in rats. The 

neurological effects were consistent with transient neurotoxicity affecting primary 

sensorimotor and gait functions. At all doses tested, there is evidence of neurotoxicity 

and neuropathology in a developmental range-finding study in rabbits. Also in the rabbit 

developmental range-finding study ataxia, hypoactivity, and neuropathology were 

observed. However, the 90-day neurotoxicity study in rats did not result in any 

significant neurotoxicity; other dietary studies in the rat, mouse and dog also did not 

show evidence of neurotoxicity.

An immunotoxicity study is also required as a part of the new data requirements in the 40 

CFR Part 158 for conventional pesticide registration. OPP is conducting an independent 

retrospective analysis of more than 120 immunotoxicity studies submitted to Agency. 

Preliminary findings of OPP’s retrospective analysis suggest that immunotoxicity studies 

have not yet provided lower PoDs than are selected from other guideline experimental 

toxicology studies and thus, so far, immunotoxicity studies would not have impacted the 

Agency’s risk assessments. The OPP retrospective analysis is anticipated to be completed 

in the summer of 2012. In the interim, HED recommends that the immunotoxicity 

continue to be required for registration and registration review chemicals.

The Points of Departures and toxicological endpoints of concern for the overall risk 

assessment (dietary and occupational) are presented in Table 6. 

Endocrine Disruption

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, 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), prosulfuron 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 
Page 6 of 22

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. 

Prosulfuron is not among the group of 58 pesticide active ingredients on the initial list to 

be screened under the EDSP. Accordingly, as part of registration review, EPA will issue 

future EDSP orders/data call-ins, requiring the submission of EDSP screening assays for 

prosulfuron. For further information on the status of the EDSP, the policies and 

procedures, the list of 67 chemicals, future lists, the test guidelines and the Tier 1 

screening battery, please visit our website: http://www.epa.gov/endo/.

Conclusions for Hazard Identification/Toxicology

The toxicology database for prosulfuron is complete at the present time with the 

exception of an immunotoxicity study. Upon receipt of the required toxicity study, HED 

may reevaluate the points of departure and uncertainty factors for the dietary and 

occupational exposure assessments. 

Residue Chemistry

The existing residue chemistry database for prosulfuron is adequate for risk assessment 

purposes; no additional data are required at this time. The qualitative nature of the 

residue(s) of prosulfuron in plants is considered adequately understood; based on 

acceptable metabolism studies and the most recently submitted rotational crop studies on 

root and leafy vegetables and small grains. Outstanding deficiencies previously noted 

(DP Barcode: D242049 dated 04/04/2000, Case: 014396) were resolved with the 

submission and acceptance of the storage stability data. The qualitative nature of the 

residue(s) of prosulfuron in animals is adequately understood based on the metabolism 

studies in ruminants and poultry. Based on the cow and chicken feeding studies, meat, 

milk, poultry, and egg tolerances are not required. There is no reasonable expectation of 

residues in livestock commodities (40CFR§6(a)(3)). Adequate high-performance liquid 

chromatography (HPLC) methods are available for enforcing tolerances for prosulfuron 

residues in plant commodities. 

Conclusions for Residue Chemistry

The existing residue chemistry database for prosulfuron is complete and adequate for risk 

assessment purposes. 
Page 7 of 22

Dietary Exposure and Risks

An unrefined chronic dietary (food and water) risk assessment and an acute dietary risk 

assessment was completed for prosulfuron (B. Hanson, D370557, 10/20/2009). These 

assessments were performed using the Dietary Exposure Evaluation Model (DEEMFCIDTM, Version 2.03) which uses food consumption data from the U.S. Department of 

Agriculture’s Continuing Surveys of Food Intakes by Individuals (CSFII) from 1994-

1996 and 1998. In these assessments, HED concluded that there is a reasonable certainty 

that no harm will result to the general population, infants, and children from chronic and 

acute dietary exposure to prosulfuron. The chronic and acute dietary exposure for food 

and water was no greater than 1% of the cPAD or the aPAD for all population groups.

Cancer dietary exposure estimates are not required for prosulfuron.

Drinking Water

The drinking water residues used in the dietary risk assessment were provided by the 

Environmental Fate and Effects Division (EFED) and summarized in the following 

memorandum: ―Drinking Water Exposure Assessment for Prosulfuron Usage on Small 

Grains and Corn,‖ (DP Number: 326831, Barrett, 11/20/2006) and incorporated directly 

into this dietary assessment. The Screening Concentration in Ground Water (SCIGROW) model was used to estimate ground water concentrations and the Pesticide Root 

Zone Model (PRZM) and Exposure Analysis Modeling System (EXAMS) models were 

used to estimate surface water concentrations.

Conclusions for Dietary Exposure and Risk Assessment

The dietary exposure database is adequate to support the existing registrations. 

Residential Exposure and Risks

There are no residential uses for prosulfuron, therefore, a residential exposure assessment 

will not be required. 

Conclusions for Residential Exposure and Risk Assessment

Currently, there are no uses for prosulfuron that would result in direct residential 

exposure. However, residential bystander inhalation exposures resulting from off-site 

transport (e.g., spray drift or volatilization) may occur as a result of applications of 

prosulfuron. The Agency is in the process of evaluating these types of exposures and 

may, as appropriate, develop policies and procedures to identify the need for and, 

subsequently, the way to incorporate post-application inhalation exposure into the 

Agency's risk assessments. The need for a bystander inhalation risk assessment for 

prosulfuron will be examined during registration review.

Aggregate Risk Assessment
Page 8 of 22

The aggregate risk assessment evaluates the combined risk from dietary exposure (food 

and water) and any non-occupational (residential) uses. There are no registered 

residential uses of prosulfuron; therefore, the aggregate assessments only reflect potential 

food and drinking water exposure and are equivalent to the dietary assessments. The 

chronic dietary exposure risks were <1% cPAD; therefore, there are no aggregate risk 

concerns. 

Conclusions for Aggregate Exposure and Risk Assessment

Updated aggregate exposure and risk assessments may be required under registration 

review if toxicological endpoints change or other new data are received by the Agency 

which impact dietary exposure estimates.

Occupational Exposure and Risks

Prosulfuron is a selective herbicide to be used for ground or aerial spray treatment for 

weed control in several crops. Prosulfuron may be applied to field corn (grown for grain, 

silage, or seed), popcorn, grain sorghum (milo), wheat, barley, rye oats, triticale, proso 

millet, and following small grain harvest. Prosulfuron is applied after emergence of both 

crop and weeds for the control of broadleaf weeds and post-emergence to weeds 

following small grain harvest. In addition, pre-emergence applications can be used in 

some areas for broadleaf weed control in sorghum. Prosulfuron is marketed as a waterdispersible granule and as a technical chemical used for formulation only. 

Occupational Handlers

In 1995, HED conducted an occupational and residential exposure assessment for small 

grains. HED determined that the MOEs (ranged from 1,000 to 8,833) were not of 

concern to mixers/loaders and applicators (i.e., MOEs ≥100). (C. Lewis, DP 219775, 

10/30/95).

In 1995, HED conducted an occupational and residential exposure assessment for corn. 

HED determined that the MOEs (ranged from 3,118 to 12,045) as a result of the 

mixing/loading and application of prosulfuron by workers do not exceed HED’s level of 

concern (i.e., MOEs ≥100). (B. Madden, 5/1/95).

Occupational Post-application

An occupational post-application exposure or risk estimate was not performed for 

prosulfuron because it is not required at this time. Based on the toxicity database, no 

appropriate dermal endpoint was identified.

Since prosulfuron is classified as Toxicity Category III for acute oral and acute dermal, 

Toxicity Category IV for acute inhalation, primary eye irritation, and primary skin 

irritation, the default Worker Protection Standard Restricted Entry Interval (REI) is 12 

hours. 
Page 9 of 22

Conclusions

The occupational exposure database is adequate to support the registration review process 

for prosulfuron. No new handler or post-application worker studies are needed at this 

time. Updated occupational handler exposure assessments may be required under 

registration review based upon revisions to the Agency’s scenario-specific surrogate 

handler exposure data (http://www.epa.gov/pesticides/science/handler-exposuretable.pdf). A revised occupational handler and a post-application assessment may also be 

needed if toxicological endpoints change or other new data are received by the Agency 

which impact exposure estimates.

Human Studies

Prosulfuron risk assessments rely in part on data from studies in which adult human 

subjects were intentionally exposed to a pesticide or other chemical. Studies such as the 

Pesticide Handlers Exposure Database, Outdoor Residential Exposure Task Force, and 

Agricultural Handler Exposure Task Force have been reviewed by the Agency and found 

on the basis of available evidence to have been neither fundamentally unethical nor 

significantly deficient relative to standards of ethical research conduct prevailing when 

they were conducted. There is no barrier in EPA's "Protection of Human Subjects" 

regulation to reliance on these studies.

Public Health and Pesticide Epidemiology Data

An updated review of prosulfuron incident reports was recently prepared by HED (S. 

Recore, D397848, 1/3/2012). For this evaluation, the OPP Incident Data System (IDS) 

was consulted for pesticide incident data on the active ingredient prosulfuron. 

The IDS includes reports of alleged human health incidents from various sources, 

including mandatory Federal Insecticide, Fungicide and Rodenticide Act (FIFRA) 

Section 6 (a) (2) reports from registrants, other federal and state health and environmental 

agencies and individual consumers. IDS contains reports from across the U.S. and most 

incidents have all relevant product information recorded. Reports submitted to the IDS 

represent anecdotal cases or allegations only, unless otherwise stated. IDS records 

incidents resulting in higher severity outcomes in more detail, in a module called the 

Main IDS module. This system stores incident data for death, major and moderate 

incidents, and it includes more details about the location, date and nature of the incident.

For the Main IDS, from January 1, 2006 to December 14, 2011 there are no cases

reported that involve the active ingredient prosulfuron. In the Aggregate IDS, from 

January 1, 2006 to December 14, 2011, there is 1 incident reported for prosulfuron. 

Because it falls within the categories reported as counts (which includes minor, unknown 

or no effects), there is no unique report that provides details about the incident and single 

chemical incidents are not distinguished from multiple chemical incidents; however, a 

high frequency of incidents indicates there is a high potential for exposure and vice versa. 
Page 10 of 22

For prosulfuron, there appears to be a low potential for exposure. Prosulfuron is not 

included in the Agricultural Health Study (AHS), and therefore, does not provide 

information for this report. 

Based on the low frequency and severity of incident cases, there does not appear to be a 

concern at this time that would warrant further investigation. The Agency will continue to 

monitor the incident information and if a concern is triggered, additional analysis will be 

included during registration review.

Tolerance Assessment and International Harmonization

Tolerances are established under 40 CFR §180.481 for residues of the herbicide 

prosulfuron parent, in or on a variety of food and feed crops (see Table 10). These 

tolerances are based on the residue analysis of prosulfuron. There are currently no 

established or proposed Codex, Canadian, or Mexican maximum residue limits (MRLs) 

for prosulfuron. 

The current tolerance expression as listed in the 40 CFR §180.481 has not been updated 

to reflect current HED policies. The tolerance expression will need to be revised during 

the registration review process. The revised tolerance expression should be as follows: 

“Tolerances are established under 40 CFR §180.481 for residues of the herbicide 

prosulfuron, including its metabolites and degradates, in or on the following 

commodities. Compliance with the tolerance levels specified is to be determined by 

measuring only prosulfuron parent [1-(4-methoxy-6-methyl-1, 3,5-triazin-2-yl)-3-[2-

(3,3,3-trifluoropropyl)-phenylsulfonyl]-urea ] in or on the commodity”.

Environmental Justice

Potential areas of environmental justice concerns, to the extent possible, were considered 

in this human health risk assessment, in accordance with U.S. Executive Order 12898, 

"Federal Actions to Address Environmental Justice in Minority Populations and LowIncome Populations," 

http://www.epa.gov/compliance/resources/policies/ej/exec_order_12898.pdf. The Office 

of Pesticide Programs (OPP) typically considers the highest potential exposures from the 

legal use of a pesticide when conducting human health risk assessments, including, but 

not limited to, people who obtain drinking water from sources near agricultural areas, the 

variability of diets within the U.S., and people who may be exposed when harvesting 

crops. Should these high exposures indicate potential risks of concern, OPP will further 

refine the risk assessments to ensure that the risk estimates are based on the best available 

information.

Cumulative Risk Assessment

At this time, EPA does not have available data to determine whether prosulfuron has a 

common mechanism of toxicity with other substances. EPA has not made a common 

mechanism of toxicity finding as to prosulfuron and any other substances, and 

prosulfuron does not appear to produce a toxic metabolite produced by other substances 
Page 11 of 22

which have tolerances in the U.S. Therefore, EPA has not assumed that prosulfuron has 

a common mechanism of toxicity with other substances.

Data Requirements

HED does not anticipate that additional residue chemistry, toxicology or 

occupational/residential exposure data will be required for the prosulfuron registration 

review process, with the exception of the following studies listed below:

Immunotoxicity Study (OPPTS 870.7800)
Page 12 of 22

Table 1. Prosulfuron Nomenclature.

Compound

Common name Prosulfuron 

IUPAC name 1-(4-methoxy-6-methyl-1,3,5-triazin-2-yl)-3-[2-(3,3,3-trifluoropropyl)-

phenylsulfonyl]-urea

CAS name Benzenesulfonamide, N-[[(4-methoxy-6-methyl-1,3,5-triazin-2-

yl)amino]carbonyl]-2-(3,3,3-trifluoropropyl)-

CAS registry number 94125-34-5

Table 2. Physicochemical Properties of the Technical Grade Prosulfuron

Parameter Value Reference

Melting point/range 155°C MSDS

pH Not Applicable

Bulk density (g ml-1)/Specific gravity 1.45

Water solubility (g/L) at 25 oC 4.0 at pH 6.8

Solvent solubility (g/L) at room 

temperature

Acetone: 160 (purity: 95.1 %)

Toluene : 6.1

Dichloromethane : 180

Ethyl acetate : 56

n-Hexane : 0.006

Ethanol : 8.4

n-octanol :1.4

Vapor pressure < 3.5x10-6 Pa at 25 °C

Dissociation constant, pKa pKa = 3.76

Octanol/water partition coefficient

(log Pow)

pH5 : 1.5 at 25°C

UV/visible absorption L mol-1cm-1ε = 21645 l x mol-1x cm-1at λ max = 227.5 nm

shoulder at 250 nm

No absorption >290 nm
Page 13 of 22

Table 3. Prosulfuron Toxicology Data Requirements

Test Technical

Required Satisfied

870.1100 Acute Oral Toxicity.......................................................

870.1200 Acute Dermal Toxicity..................................................

870.1300 Acute Inhalation Toxicity..............................................

870.2400 Primary Eye Irritation....................................................

870.2500 Primary Dermal Irritation ..............................................

870.2600 Dermal Sensitization .....................................................

yes

yes

yes

yes

yes

yes

yes

yes

yes

yes

yes

yes

870.3100 Oral Subchronic (rodent)...............................................

870.3150 Oral Subchronic (nonrodent).........................................

870.3200 21-Day Dermal..............................................................

870.3250 90-Day Dermal..............................................................

870.3465 90-Day Inhalation..........................................................

yes

yes

yes

no

no

yes

yes

yes

-

-

870.3700a Developmental Toxicity (rodent)...................................

870.3700b Developmental Toxicity (nonrodent) ............................

870.3800 Reproduction .................................................................

yes

yes

yes

yes

yes

yes

870.4100a Chronic Toxicity (rodent)..............................................

870.4100b Chronic Toxicity (nonrodent)........................................

870.4200a Oncogenicity (rat)..........................................................

870.4200b Oncogenicity (mouse) ...................................................

870.4300 Chronic/Oncogenicity ...................................................

yes

no

yes

yes

yes

yes

-

yes

yes

yes

870.5100 Mutagenicity—Gene Mutation - bacterial.....................

870.5xxx Mutagenicity—Structural Chromosomal Aberrations...

870.5xxx Mutagenicity—Other Genotoxic Effects.......................

yes

yes

yes

yes

yes

yes

870.6100a Acute Delayed Neurotox. (hen).....................................

870.6100b 90-Day Neurotoxicity (hen) ..........................................

870.6200a Acute Neurotox. Screening Battery (rat) .......................

870.6200b 90-Day Neuro. Screening Battery (rat)..........................

870.6300 Develop. Neuro .............................................................

no

no

yes

yes

no

-

-

yes

yes

-

870.7485 General Metabolism ......................................................

870.7600 Dermal Penetration........................................................

870.7800 Immunotoxicity...............................................

yes

no

yes

yes

-

no
Page 14 of 22

Table 4 Acute Toxicity of Prosulfuron Technical

Guideline No. Study Type MRID # Results Toxicity Category

870.1100 Acute Oral 42685215 LD50 = 986 mg/kg III

870.1200 Acute Dermal 42685216 LD50 > 2000 mg/kg III

870.1300 Acute Inhalation 42685217 LC50 = 5.467 mg/L IV

870.2400 Primary Eye 

Irritation

42685218 Minimal irritant IV

870.2500 Primary Skin 

Irritation

42685219 Non-irritant IV

870.2600 Dermal 

Sensitization

42685220 Non-sensitizer N/A

Table 5. Prosulfuron Subchronic, Chronic and Other Toxicity Profile

Guideline No./ Study Type MRID No. (year)/ 

Classification 

/Doses

Results

82-1 870.3100

90-Day oral toxicity rats

42685232

Dietary levels of 0, 

5, 50, 500, 4,000 or 

8,000 ppm. Mean 

daily doses were 0, 

0.31, 3.1, 31, 255, or 

522 mg/kg/day for 

males and 0, 0.32, 

3.4, 35, 268, or 512 

mg/kg/day for .

The LOAEL is 500 ppm for males, based 

on reduced body weight and body weight 

gain (13%); and 4,000 ppm for females, 

based on reduced body weight, body 

weight gain, food consumption, and food 

efficiency. In addition, statistically 

significant reductions in 5'nucleotidase 

activity at > 4,000 ppm and reduced 

triglycerides at 8,000 were observed in 

males, although it was unclear whether 

these changes were related to treatment. 

The NOAEL is 50 ppm (3.1 mg/kg/day) 

for males and 500 ppm (35 mg/kg/day) for 

females.

870.3100 

90-Day feeding - mouse.

42685234

Dietary levels of 0, 

15, 500, 1750, 3500, 

or 7000 ppm. Mean 

daily doses were 0, 

2.0, 69.3, 234, 504, 

969 mg/kg/day for 

males and 0, 2.9, 

91.3, 293, 606, and 

1400 mg/kg/day for 

females.

At higher dose levels, degenerative 

vacuolation of the heart was observed in 

males at > 3500 ppm and in females at 

7000 ppm. The incidence of centrilobular 

hypertrophy observed in the liver was 

statistically significant at > 1750 in males 

and > 3500 in females. The 

histopathological findings in the liver 

correlated with the statistically significant 

increased relative liver (to brain and/or 

body) weight observed in both sexes at > 

1750 ppm. The LOAEL is 500 ppm (69.3 

mg/kg/day) for males, based on 
Page 15 of 22

Table 5. Prosulfuron Subchronic, Chronic and Other Toxicity Profile

Guideline No./ Study Type MRID No. (year)/ 

Classification 

/Doses

Results

statistically significant decreased albumin 

and total bilirubin and statistically 

significant increased absolute and relative 

liver (to brain and/or body) weights. The 

LEL is 1750 for females, based on 

statistically significant increased relative 

liver (to brain and body) weights, 

statistically significant increased 

hematocrit and mean corpuscular volume, 

and decreased mean corpuscular 

hemoglobin concentration. The NOAEL is 

15 ppm (2.0 mg/kg/day) for males; 500 

ppm (91.3 mg/kg/day) for females.

82-1 870.3100 

90-Day feeding – dog.

42685230

via the diet at dose 

levels of 0, 15, 150, 

1500, or 3000 ppm 

for 90 days. The 

equivalent average 

daily intake of test 

material was 0, 0.54, 

5.3, 57, or 110 

mg/kg/day (males) 

and 0, 0.59, 6.5, 54, 

or 120 mg/kg/day 

(females). 

At the highest dose tested, two males 

displayed myocardial necrosis with 

fibrosis and dystrophic mineralization in 

the ventricular and papillary muscles and 

one female displayed myocardial 

degeneration. The NOAEL is 150 ppm 

(5.3 mg/kg/day) and the LOAEL is 1500 

ppm (54 mg/kg/day) based on decreased 

bodyweight gain and feed efficiency as 

well as hematological and hepatic toxicity 

in both males and females.

82-2 870.3200

21-day dermal toxicity study - rabbits

42685235

Doses of 0, 10, 100, 

500 or 1,000 

mg/kg/day CGA152005 Technical, 

were applied to the 

clipped backs of 

Chbb:NZW rabbits 

for 6 hours/day, 7 

ays/week, for 3 

weeks.

There was increased absolute and relative 

liver weights in both sexes at 500 and 

1000 mg/kg/day. However, these findings 

were not considered sufficient to establish 

a systemic toxicity LOAEL. The increased 

liver weights, however, were considered 

indicative of dermal absorption of CGA152005. Based on the absence of any 

significant dermal or systemic effects at 

the highest dose tested (1000 mg/kg/day), 

the NOAEL's for dermal and systemic 

effects are established at 1000 mg/kg/day. 

An LOAEL was not determined.

870.3250 90-Day dermal toxicity No study available and not required at this time. 

870.3465 90-Day inhalation toxicity No study available and not required at this time. 

83-3 870.3700

Prenatal developmental - rats.

1992. 

43159317

42700001

Sprague Dawley rats 

received either 0, 5, 

50, 200 or 400 mg 

of CGA152005/kg/day by 

gavage (technical, 

96% a.i.), from 

There was a statistically significant 

decrease in bodyweight gain at the high 

dose of 400 mg/kg/day during the 

treatment period. No other maternal 

toxicity was observed at any dose level in 

this study. The LOAEL for maternal 

toxicity = 400 mg/kg/day (highest dose 

level tested), based on decrease body 

weight gain. The NOAEL for maternal 
Page 16 of 22

Table 5. Prosulfuron Subchronic, Chronic and Other Toxicity Profile

Guideline No./ Study Type MRID No. (year)/ 

Classification 

/Doses

Results

gestation days 6 

through 15, 

inclusive

toxicity = 200 mg/kg/day. The incidence 

of skeletal alterations per litter, which 

included the incidence of extra full and 

rudimentary ribs (increase in findings of 

14th ribs) seen in the high dose group of 

400 mg/kg/day versus controls, gives 

evidence of developmental toxicity. Thus, 

the LOAEL for developmental toxicity = 

400 mg/kg/day based on skeletal findings 

(increase in findings of 14th ribs). The 

NOAEL for developmental toxicity = 200

mg/kg/day.

83-3 870.3700

Prenatal developmental - rabbits 

1992

42685239

42685238

43159318

New Zealand White 

rabbits receive either 

0, 1, 10, or 100 mg 

of CGA152005/kg/day by 

gavage (96% a.i.), 

from gestation days 

7 through 19, 

inclusive. 

The LOAEL for maternal toxicity is > 100 

mg/kg/day (highest dose level tested) and 

the NOAEL for maternal toxicity > 100 

mg/kg/day (HDT). A developmental 

toxicity LOAEL has not been determined 

in this study. Therefore, the LOAEL for 

developmental toxicity is > 100 mg/kg/day 

(highest dose level tested) and the NOAEL 

for developmental toxicity > 100 

mg/kg/day (HDT). No effects were noted 

at the highest dose level tested, 100 

mg/kg/day, but this should not be 

considered a definitive NOAEL since the 

maternal animals were not adequately 

challenged, and a limit dose was not 

utilized in this study.

83-3 870.3700

Prenatal developmental - rabbits 

1996

43953506

New Zealand White 

rabbits received 

dosages of CGA152005 technical 

(96% a.i.) by gavage 

at dose levels of 0, 

20, 100 and 200 

mg/kg/day on 

gestation days 7 to 

19

Available data support an LOAEL for 

maternal toxicity of 100 mg/kg/day based 

on increases in abortion, decreases in food 

consumption, and in mean body weight 

gain. The NOAEL is 20 mg/kg/day. A 

dose-related increase in runts and small 

fetuses was observed in the 100 and 200 

mg/kg/day groups. Fetal weights were 

reduced and skeletal anomalies/delayed 

ossification increased. Based upon the 

dose-related increase in runts and small 

fetuses and the skeletal effects, an LOAEL 

for developmental toxicity can be 

established at 200 mg/kg/day. An NOAEL 

for developmental toxicity can be 

established at 100 mg/kg/day.

83-4 870.3800

Multigeneration Reproduction - rat 

1992

42700002

Sprague-Dawley rats 

received either 0, 10, 

200, 2000, or 4000 

ppm (0, 0.67, 13.3, 

136, and 278 

mg/kg/day for P0 

The NOAEL for parental toxicity is 200 

ppm (13.3 mg/kg/day for males and 15.3 

mg/kg/day for females). The LOAEL for 

parental toxicity is 2000 ppm (136 

mg/kg/day for males and 152 mg/kg/day 

for females), based upon decreased mean 

body weights and body weight gain 
Page 17 of 22

Table 5. Prosulfuron Subchronic, Chronic and Other Toxicity Profile

Guideline No./ Study Type MRID No. (year)/ 

Classification 

/Doses

Results

males and 0, 0.76, 

15.3, 152, and~3l1 

mg/kg/day for P0 

females during the 

premating growth 

periods, 

respectively) of 

CGA-152005 

(99.1% a.i.) mixed 

in the feed.. 

observed in the P0 and P1 generation 

animals. 

Reproductive performance of the P1 

generation to produce the F2 litters was 

slightly affected at the 4,000 ppm dose 

level with decreases noted in the Fertility, 

Gestation and Parturition Indices. On day 

4 of lactation, mean litter size was reduced 

to a statistically significant level (p < 0.05) 

with a mean of 13 pups per litter at 4000 

ppm versus 14.7 in the controls. By day 14 

of lactation, pups at both the 2000 and 

4000 ppm levels had statistically 

significantly reduced mean pup weights. 

Therefore, in both generations, an effect 

during lactation was apparent.

The NOAEL for reproductive toxicity is 

established at 200 ppm (13.3 mg/kg/day 

for males and 15.3 mg/kg/day for 

females). The LOAEL for reproductive 

toxicity is established at 2000 ppm (136 

mg/kg/day for males and 152 mg/kg/day 

for females), based upon decreased pup 

weights observed in both the Fl and F2 

offspring.

83-1 870.4100 Chronic toxicity 

rodents

Refer to 870.4300 rat chronic feeding/carcinogenicity study below

83-1 870.4100

Chronic toxicity dogs. 

43159314 

43387705

Diet concentrations 

at 0, 10, 60, 600 or 

1200 ppm (0.3, 2.0, 

18.6 or 41.0 

mg/kg/day, males 

and 0, 0.3, 1.8, 20.2 

or 48.8 mg/kg/day, 

females).mg/kg/day

The LOAEL is 600 ppm (18.6 mg/kg/day, 

males), based on hematologic and clinical 

chemistry effects (females) and incidence 

of lipofuscin accumulation in liver (both 

sexes). The NOAEL is 60 ppm (1.8 

mg/kg/day, females).

83-2 870.4200

Carcinogenicity mice. 

1995

18-months

43159316

43387706

(Crl:CD-(ICR)BR), 

mice were admin 0, 

15, 700, 3500 or 

7000 ppm of CGA152005 technical in 

the diet. Compound 

consumption was: 0, 

1.71, 81.4, 410 and 

832 mg/kg/day in 

males; 0, 2.11, 100, 

508, and 1062 

mg/kg/day in 

The systemic toxicity LOAEL is 3500 

ppm (410 mg/kg/day in males and 508 

mg/kg/day in females), based on slightly 

decreased body weight gain in females. 

The systemic toxicity NOAEL is 700 ppm 

(81.4 mg/kg/day in males and 100 

mg/kg/day in females). There appeared to 

be no increase in the incidence of 

neoplasia in treatment groups when 

compared to controls. 
Page 18 of 22

Table 5. Prosulfuron Subchronic, Chronic and Other Toxicity Profile

Guideline No./ Study Type MRID No. (year)/ 

Classification 

/Doses

Results

females.

83-5 870.4300. Combined chronic 

feeding and carcinogenicity study -

rats

1994

2 - years

42700003

43159321

(CrL:CD(SD)BR), 

rats were 

administered 0,10, 

200, 2000 or 4000 

ppm (0.4, 7.9, 79.9 

and 160.9 

mg/kg/day for males 

and 0.5, 9.2, 95.7 

and 205.8 

mg/kg/day for 

females, 

respectively) of 

technical CGA152005 (a.i. 99.1%) 

in the diet.

The systemic NOAEL is 200 ppm (7.9 

mg/kg/day, males and 9.2 mg/kg/day, 

females). The systemic LOAEL is 2000 

ppm (79.9 mg/kg/day, males and 95.7 

mg/kg/day, females), based on decreased 

body weight and body weight gain during 

the first months to 1 year of the study, 

decreased food consumption (females), 

hematopoietic system effects (males), and 

possibly increased GGT with decreases in 

liver, kidney and adrenal weight (females).

Increases in the incidence of mammary 

adenocarcinomas in females was observed 

at 2000 ppm (31.9%; p < 0.5) and 4000 

ppm (26.3%; NS) compared to controls 

(17.5%). Mammary gland adenomas were 

also slightly increased at 2000 ppm and 

4000 ppm (4.3% and 2.5% vs. 0%, 

controls). Slight increases in the incidence 

of benign testicular interstitial cell tumors 

(significant trend only) were also observed 

at 2000 ppm (8.6%) and 4000 ppm (5.0%) 

compared to controls (1.6%). 

81-8 870.6200

Acute neurotoxicity screening battery

Functional observational battery and 

motor activity tests were conducted 

pretreatment, on the day of dosing 

(peak effect, 3 hr post-dosing) and on 

Day 7 and 14 post-dosing. Neural 

tissues from 5 control and high dose 

animals/sex and brain levels 4 and 5 

from all animals were examined 

microscopically.

43387703

Hsd:SpragueDawley rats received 

0, 10, 250, 500 or 

1000 mg CGA152005 (technical, 

99.1% a.i.)/kg body 

weight by gavage in 

aqueous 3% corn 

starch/-0.5% Tween 

80 (20 ml/kg). 

The LOAEL is 250 mg/kg/day, based on 

reduced motor activity and body 

temperature in males and abnormal gait in 

females. The NOAEL is 10 mg/kg.

81-8 870.6200

Subchronic neurotoxicity screening 

battery – 90 day

43387704

Rats were fed diets 

containing 0, 10, 

200, 2500, 5000 

(high dose, females 

only) or 10,000 

(high dose, males 

only) ppm prosulfuron technical. The 

equivalent average 

daily test material 

intakes were 0, 0.6, 

12.1, 147 or 628 

mg/kg/day, males; 0, 

0.6, 12.5, 157 or 313 

mg/kg/day, 

The LOAEL for systemic toxicity is 2500 

ppm, based on slightly reduced body 

weight gain in males. The NOAEL is 200 

ppm. The NOAEL for neurotoxicity is 

>10,000 ppm (males) or >5000 ppm 

(females).
Page 19 of 22

Table 5. Prosulfuron Subchronic, Chronic and Other Toxicity Profile

Guideline No./ Study Type MRID No. (year)/ 

Classification 

/Doses

Results

females).

85-1 870.7485

Metabolism and pharmacokinetics -

rat

43159326

Rats were 

administered 

[phenyl-14C] 

prosulfuron as a 

single oral dose of 

0.5 mg/kg, a single 

i.v. dose of 0.5 

mg/kg, a single oral 

dose of 400 mg/kg 

and a single oral 

dose of [phenyl14C] prosulfuron 

following 14 days of 

repeated dosing with 

0.5 mg/kg of 

nonlabeled 

compound.

Approximately 90% of the administered 

dose was excreted during the first 48 

hours. At 400 mg/kg, a greater proportion 

of the administered dose was excreted in 

the feces (33-36%) compared to urine (61-

71%). Females usually excreted more of 

the dose in the urine (79-91%) than males 

(66-79%). The parent compound 

represented 8-27% of the total activity in 

the urine of females and 5-9% in males, 

whereas in the feces there was 10-16% of 

the parent compound in females and 5-6% 

in males. Fifteen urinary metabolites were 

determined and 13 similar metabolites 

were confirmed in feces. Tissue levels 

were low. No measurable amount of 

radioactivity was found in most tissues 

168 hours post-dosing in animals at 0.5 

mg/kg. The major routes of metabolism 

occurred via hydroxylation at side chains 

and phenyl ring of the trifluoropropyl side 

chain, hydrolysis of the phenylsulfonylurea link and oxidative/hydrolytic 

cleavage of the triazine ring system. The 

major metabolite (47% to 60% of urinary 

radioactivity at 0.5 mg/kg) was formed by 

hydroxylation of the triazinyl methyl 

group. At the 0.5 mg/kg level, metabolism 

was not affected by route of 

administrationpositions and Odemethylation of the triazyl methoxy 

group. Minor routes of metabolism 

included unsaturation

85-1 870.7485

Metabolism and pharmacokinetics -

rat

43159322 

43159323

rats were 

administered 

[triazine-4-14C] 

prosulfuron as a 

single oral dose of 

0.5 mg/kg, a single 

i.v. dose of 0.5 

mg/kg, a single oral 

dose of 400 mg/kg 

and a single oral 

dose of [triazine-4-

14C] prosulfuron 

following 14 days of 

repeated dosing with 

0.5 mg/kg of 

Approximately 90% of the administered 

dose was excreted within 48 hours postdosing. Tissue radioactivity was low, less 

than 0.91% of the administered dose. The 

metabolite profile for each sex was similar 

regardless of the route of administration. 

However, females tended to excrete more 

radioactivity in the urine and less in the 

feces than males. The metabolites in the 

greatest concentration in the urine were #2 

(hydroxylation of triazinyl methyl group) 

and #11 (parent compound) along with #1 

(O-demethylated methoxy group) and #3 

(hydroxylation of trifluoropropyl group). 

Females excreted more parent compound 

than males. Males excreted more of the 

hydroxylated metabolites and more 
Page 20 of 22

Table 5. Prosulfuron Subchronic, Chronic and Other Toxicity Profile

Guideline No./ Study Type MRID No. (year)/ 

Classification 

/Doses

Results

nonradiolabeled 

compound.

metabolites with a double bond on the 

trifluoropropyl group. Urinary metabolite 

#3 was greater at 400 mg/kg than 0.5 

mg/kg, especially in males. It is believed 

that O-demethylation of the methoxy 

group and hydroxylation of the triazinyl 

methyl group are the primary metabolic 

pathways; while hydroxylation at various 

sites of the trifluoropropylbenzene moiety 

is a slower process that increases in 

importance as the primary pathways 

approach saturation.

85-2 Dermal Absoprtion No study available and not required at this time.

Table 6. Summary of Toxicological Doses and Endpoints for Prosulfuron for Use in 

Dietary and Occupational Human Health Risk Assessments

Summary of Toxicological Endpoints Prosulfuron for Use in Human Health Risk Assessment

Exposure

Scenario

Dose Used in Risk 

Assessment,

UF

FQPA SF and Level of 

Concern for Risk 

Assessment

Study and Toxicological Effects

Acute Dietary

All populations

NOAEL = 10 

mg/kg

UF = 100

Acute RfD = 0.1 

mg/kg/day

FQPA SF = 1X

aPAD = 0.1 

mg/kg/day

Acute Neurotoxicity Study - Rat

LOAEL = 250 mg/kg/day, based on 

abnormal gait in females.

Chronic Dietary

All populations

NOAEL= 5.3 

mg/kg/day

UF = 100

Chronic RfD = 

0.053 mg/kg/day

FQPA SF = 1X

cPAD = 0.053 

mg/kg/day

Subchronic Oral Toxicity Study - Dog

LOAEL = 54 mg/kg/day, based on 

decreased body-weight gain and feed 

efficiency, hematological findings and 

hepatotoxicity in both sexes.

Short- (1-30 days) 

Intermed-Term

(1-6 months) and 

Long-Term (>6 

months) Dermal 

Not required based on the fact that no hazard was identified in the dermal study at dose 

levels as high as the limit dose (1000 mg/kg/day).

Short- (1-30 days), 

Intermed-(1- 6 

months) and LongTerm (> 6 months) 

Inhalation

NOAEL = 5.3 

mg/kg/day

FQPA SF = 1X Subchronic Oral Toxicity Study - Dog

LOAEL = 54 mg/kg/day, based on 

decreased body-weight gain and feed 

efficiency, hematological findings and 

hepatotoxicity in both sexes.
Page 21 of 22

Summary of Toxicological Endpoints Prosulfuron for Use in Human Health Risk Assessment

Exposure

Scenario

Dose Used in Risk 

Assessment,

UF

FQPA SF and Level of 

Concern for Risk 

Assessment

Study and Toxicological Effects

Cancer

(oral, dermal, 

inhalation)

Prosulfuron is classified as ―Not Likely to Be Carcinogenic to Humans” based on the lack 

of evidence of carcinogenicity in mice and rats and no concern for mutagenicity. 

1 UF = uncertainty factor, FQPA SF = Special FQPA SF, NOAEL = no observed adverse effect level, 

LOAEL = lowest observed adverse effect level, PAD = population adjusted dose (a = acute, c = chronic) 

RfD = reference dose

Table 7. Prosulfuron Tolerances 40 §180.481 Parts per million

Grain, cereal, forage, fodder, and straw, group 16, except rice, fodder 0.01

Grain, cereal, forage, fodder, and straw, group 16, except rice, forage 0.10

Grain, cereal, forage, fodder, and straw, group 16, except rice, hay 0.20

Grain, cereal, forage, fodder, and straw, group 16, except rice, straw 0.02

Grain, cereal, group 15, except rice 0.01

Table 8: HED Memoranda Relevant to Registration Review

Author Barcode Date Title

B. Hanson D370557 10/20/2009 Prosulfuron: Human Health 

Risk Assessment (Revised)

B. Hanson D299767 12/19/2006

Prosulfuron: Acute and 

Chronic Dietary (Food and 

Drinking Water) Exposure 

Assessment

L. Taylor HED Doc 0054301 08/16/2006

Health Effects Division 

Toxicology/Hazard Assessment 

Update for Prosulfuron Human 

Health Risk Assessment

G. J. 

Herndon D242049 04/04/2000

PP#5F4469. Prosulfuron in or 

on Cereal Grains (Except Rice) 

and Animal Commodities

M. Bonner HED Doc 0013976 01/24/2000 Health Effects Division 

HIARC Report
Page 22 of 22

Table 8: HED Memoranda Relevant to Registration Review

Author Barcode Date Title

B. Madden None 05/01/1995

Health Effects Division Risk 

Assessment for Use of 

Prosulfuron in/on Corn

C. Lewis D219775 10/30/1995 Exposure Assessment for Use 

of Prosulfuron on Small Grains