UNITED STATES ENVIRONMENTAL PROTECTION AGENCY 

WASHINGTON, D.C. 20460 

MEMORANDUM 

Date: August 8, 201 4 

O FFICE OF 

CHEMICAL FI TY ANI> 

POLLUTION PREVENTION 

SUBJECT: Triallate. Human Health Risk Assessment Scoping Document in Support of 

Registration Review 

PC Code: 078802 

Decision No.: 489685 

Petition No.: Not Applicable 

Risk Assessment Type: Single Chemical 

TXR No.: Not Applicable 

MRID No.: None 

FROM: 

THRU: 

TO: Katherine St. Clair 

DP Barcode: 0419239 

Registration No.: Not Applicable 

Regulatory Action: Registration Review Scoping 

Case No.: Not Applicable 

CAS No.: 2303-17-5 

40 CFR: §180.314 

Pesticide Re-evaluation Division (7508P) 

Office of Pesticide Programs 

Attached is the Health Effects Division's (HED) human health scoping document for triallate to 

support the registration review process. 

Page 1 of 24 
Executive Summary 

The Health Effects Division (HED) has evaluated the status of the human health risk assessment 

for triallate to determine the scope of work necessary to support Registration Review. The most 

recently completed human health risk assessment (2008; D351897) was considered as part of this 

scoping exercise. 

Triallate (S-(2,3,3-trichloro-2-propen-1 -yl) .N,N-bis(l-methylethyl)carbamothioate) is a preemergent selective herbicide used on barley, lentils, peas (dried and succulent), triticale, sugar 

beets, wheat, and grass grown for seed/hay. It is used for the pre-emergent control of weeds by 

inhibiting cell division and promoting the elongation of seedling shoots in targeted plants. 

Triallate is an herbicide active ingredient in the class of thiocarbamates. Triallate is sold under 

the trade names Far-Go®, Buckle®, and Avadex® as either granular or emulsifiable concentrate 

end-use products. It is registered for use on Bermuda grass grown for seed with tolerances 

established under 40 CFR § 180.314(a) for the hay raw agricultural commodity (RAC). 

Tolerances for its regional use on barley (grain, hay & straw), sugar beets (dried pulp, roots & 

tops), peas (dry, hay, vines & succulent), and wheat (forage, grain, hay & straw) are also 

established under 40 CFR §180.314(c). Applications to crops are typically made at rates of 1.0-

1.5 lb ail A as pre-plant and post-plant soil incorporated treatments using ground or aerial 

equipment. It is applied in either the fall or spring before targeted weed species germinate. 

The toxicity database for triallate is complete and adequate for characterization of potential 

developmental, reproductive, carcinogenetic, mutagenic, and neurotoxic effects. No new 

toxicity studies have been received since the last risk assessment. During registration review of 

triallate, endpoint selection, points of departure (PODs), and uncertainty factors (UFs)/ safety 

factors (SFs) for the risk assessments will be re-evaluated based upon updated policies and 

procedures. 

The residue chemistry database is complete. The current tolerance expression should be updated 

to comply with HED's current policy on tolerance expressions during registration review. 

There are no maximum residue limits (MRLs) established for the residues oftriallate by Codex 

or Mexico. Canada has established MRLs on triallate for a nuinber of commodities which are 

harmonized with those tolerances set by the U.S. As such, there are no international 

harmonization issues. HED is not currently involved in any joint international review projects 

that involve the active ingredient, triallate. 

Currently there are no acute or chronic dietary (food and drinking water) risk estimates which are 

of concern for triallate and its metabolites. A cancer dietary risk assessment was performed 

which determined a cancer risk estimate of3.0 x 10·7 for the general U.S. population. Updated 

dietary exposure assessments for triallate may be necessary under registration review if there are 

significant changes to the drinking water estimated concentrations which will be updated by 

EFED, or if there are significant changes to the PoDs or UFs/SFs. 

There are no non-occupational (residential) uses registered for triallate. 

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Page 3 of 24

Residential bystander exposures resulting from off-site transport (i.e., spray drift or 

volatilization) may occur as a result of occupational applications of triallate. The need for a 

bystander risk assessment for triallate will be considered during registration review.

There are no current aggregate risks estimates of concern for triallate. During registration 

review, updated aggregate assessments may be conducted as required to include any significant 

change that might occur for toxicological PODs, FQPA and uncertainty factors, dietary exposure 

estimates, or estimated drinking water concentrations (EDWCs). 

The exposure database for triallate is complete. Based on the previous occupational exposure 

assessment, all of the handler (dermal and inhalation) exposure non-cancer risk estimates were 

not of concern with label required PPE. Some occupational handler cancer risk estimates with 

label required PPE are within the 10-6 to 10-4range; all risk estimates do not exceed 5 x 10-5. 

There are no post-application worker exposure non-cancer risk estimates of concern. Based on 

the previous occupational handler exposure assessment, all post-application cancer risk estimates 

do not exceed 7 x 10-6. No DFR or TTR data are required for triallate. The Worker Protection 

Standard (WPS) restricted entry interval (REI) for triallate is 12 hours. An updated occupational 

exposure and risk assessment may be required during registration review if warranted by any 

changes to policy or points of departure.

Introduction

HED has evaluated the most recent complete human health risk assessment for triallate to 

determine if sufficient data are available and if updates are needed to support registration review. 

HED has also considered updates to its toxicity, exposure and usage databases, and the latest 

Agency science policy and risk assessment methodologies. 

Triallate is a selective, pre-emergence herbicide in the class of thiocarbamates. The chemical 

structure, nomenclature, and the physical/chemical properties of triallate are presented in Appendix 

A.

Registered agricultural use sites of triallate include barley, lentils, peas (dried and succulent), 

triticale, sugar beets, wheat, and grass grown for seed/hay. Formulations include granulars and

emulsifiable concentrates.

Hazard Identification/Toxicology

The toxicology database for triallate is complete. No new animal toxicity studies have been 

submitted since the most recent HED risk assessment conducted in 2008 (D351897). It is 

recommended that the immunotoxicity study be waived (see HASPOC report, TXR#0056861, 

January 28, 2014).

Following chronic exposure, systemic toxicity in dogs was limited to an increase in liver weight 

in both sexes, increases in serum alkaline phosphatase in both sexes and increases in hemosiderin 

in the spleen at dose levels higher than 4.25 mg/kg/day. In mice, toxicities observed at the
Page 4 of 24

Lowest Observed Adverse Effect Level (LOAEL) of 60 ppm (9 mg/kg/day) included increased 

absolute liver weight, increased incidence of altered foci of the liver and hematopoiesis in the 

spleen. In rats, systemic toxicity was manifested as decreased survival in both sexes, decreased 

body weight and increased adrenal weight in males at approximately 12.5 mg/kg/day. In high 

dose males from the chronic toxicity/carcinogenicity study, the only treatment-related finding at 

interim sacrifice was linear papillary mineralization in 1/10 rats (uncommon finding in rats at 

one year and typical of alpha 2 μ-globulin-induced renal pathology). The only treatment-related 

effect noted in male Syrian hamsters was decreased serum triglycerides at the mid- and highdose levels of 300 ppm (LOAEL) and 2000 ppm.

Triallate is neurotoxic in rats based on the acute and subchronic neurotoxicity studies, the rat 

multi-generation reproduction study and the developmental neurotoxicity study. In the acute 

neurotoxicity screening study, neurotoxic signs include gait abnormalities, increased alertness, 

waddling, rocking lurching, circling movements, retropulsion, and head shaking, decreases 

followed by increases in motor activity and other symptoms at 300 or 600 mg/kg. The rat 

subchronic neurotoxicity study indicated pathological lesions in the nerve fibers of both central 

and peripheral origin, FOB changes and increased motor activity at dose levels of approximately 

33 mg/kg/day and above. In addition, head bobbling and circling movements were noted in the 

rat multi-generation reproduction study in the parental groups at 600 ppm (30 mg/kg/day). A 

special supplementary neurotoxicity study indicated that both central and peripheral 

neuropathological lesions result from triallate exposure at a dose level of 6000 ppm (295 

mg/kg/day). The developmental neurotoxicity study indicated the fetuses exposed in utero and 

during lactation displayed increased motor activity at a maternal dose of 60 mg/kg/day but there 

was no associated neuropathology. Triallate did not produce neuropathology in hens at doses up 

to 312.5 mg/kg in the acute delayed neurotoxicity study.

Analysis of whole body elimination in male and female rats indicated that 85% of the 

radiolabeled triallate was excreted within 24 hours of dosing. Most radioactivity was excreted in 

approximately equal amounts (42%) in the urine and feces of male rats after 10 days. Females 

excreted 51% in urine and 32% in feces after 10 days. Males and females retained about 0.4% of 

the dose in organs and tissues and approximately 2.0% in the remaining carcass. The distribution 

of radioactivity in both sexes indicated that the greatest amount of activity was found in the red 

blood cells followed by whole blood, spleen, kidney, liver and lung. Seven metabolites, in 

concentrations of greater than one percent, were identified in rat urine: 2,3,3-trichloro-2-

propenesulfinic acid (20-27%), N-acetyl-S-(2,2-dichloro-1-[methyl-sulfonyl) methyl]ethenyl)-Lcysteine (6-11%), (E)-S-(2 carboxy-2-chloroethenyl)-L-cysteine (4-5%), carbon dioxide (4%), 

2,3,3-trichloro-2-propene sulfonic acid; TCPSA (3-5%), (E)-3- ((carboxymethyl)thio)-2-chloro2-propenoic acid (1-3%), and 1-((3, 3, 2-trichloro-2- propenyl)thio)-beta-D-glucuronic acid. The 

remaining metabolites were found at less than 1% of the administered dose.

In the rat developmental toxicity study, the dams were more sensitive than the pups; the maternal 

toxicity NOAEL was 10 mg/kg/day and the LOAEL was 30 mg/kg/day based on deceases in 

body weight and food consumption whereas the developmental toxicity NOAEL was 30 

mg/kg/day and the LOAEL was 90 mg/kg/day based on decreased fetal weight, external 

malformations and skeletal variations.
Page 5 of 24

However, there is evidence of increased susceptibility in the prenatal developmental toxicity 

study in rabbits since the developmental effects were observed at a dose lower than the dose 

which produced maternal toxicity. Maternal toxicity manifested as increased incidence of clinical 

signs and decreased body weight gain during the dosing period at 45 mg/kg/day (LOAEL); the 

NOAEL was 15 mg/kg/day. The LOAEL for developmental toxicity was 15 mg/kg/day based on 

decreased fetal body weight and increased incidence of malaligned sternebrae; the NOAEL was 

5 mg/kg/day.

In the two-generation reproduction study, increased neonatal mortality during the F2b litter 

interval, reduced pup weights at birth during the F2b litter interval, reduced pup weights in late 

lactation for all litters, reduced pregnancy rate and shortened gestation length occurred at the 

same dose (30 mg/kg/day) which produced maternal toxicity (increased

mortality, increased incidences of chronic nephritis, head bobbing, circling movements and 

reduced body weights). The maternal and offspring toxicity NOAELs were 7.5 mg/kg/day.

In the developmental neurotoxicity study, offspring toxicity occurred at the same dose which 

produced maternal toxicity. For maternal toxicity, the NOAEL was 30 mg/kg/day and the 

LOAEL was 60 mg/kg/day based on reductions in body weight gains and food consumption. At 

60 mg/kg/day (developmental neurotoxicity LOAEL), there were several parameters affected in 

the developing offspring; reductions in body weight in both sexes, increased motor activity in

both sexes and decreases in passive avoidance latency in females. The developmental 

neurotoxicity NOAEL was 30 mg/kg/day.

Triallate is classified as a Group C, possible human carcinogen based on hepatocellular 

carcinomas in male mice, with a positive trend and borderline significance in female mice and 

increased incidence of renal tubular cell adenomas in rats. The cancer unit risk Q1* is 7.17 x 10

-2

(mg/kg/day)

-1

based on hepatocellular carcinomas in male mice. Triallate induced genotoxic

responses in several in vitro mutagenicity assays in bacteria and tumor cells (i.e. in Salmonella

typhimurium, in the mouse lymphoma forward mutation assay in L5178Y cells and in the sister

chromatid exchange assay). However, triallate was negative in two more definitive mutagenic 

assays in primary rat hepatocytes. Additionally, triallate was negative for in vivo mutagenic 

assays in mice and hamsters at doses up to 700 mg/kg/day, well above the highest POD of 60 

mg/kg/day. Therefore, the mutagenic concern of triallate in vivo is low.

Triallate is not acutely toxic via the dermal and inhalation routes. It is slightly toxic via the oral 

route and is a slight eye irritant, as well as a slight dermal irritant and a dermal sensitizer.

The FQPA factor can be reduced to 1X. A 1X FQPA Safety Factor is appropriate because (i)

the toxicology database is adequate for assessing the sensitivity of infants and children to triallate 

exposure; (ii) no quantitative or qualitative increased susceptibility was demonstrated in the

fetuses in the prenatal developmental toxicity study in rats following in utero exposure, in the 

offspring in the developmental neurotoxicity study in rats, as well as in the offspring in the twogenerational reproduction study in rats following in utero and/or postnatal exposure to triallate; 

(iii) although there is some increased susceptibility in the rabbit developmental toxicity study 

(where the developmental NOAEL of 5 mg/kg/day was lower than the maternal NOAEL of 15 

mg/kg/day), the dose-response for this effect has been adequately characterized, and the fetal 
Page 6 of 24

NOAEL was selected as a point of departure for the acute dietary, dermal and inhalation risk 

assessment and is protective of potential adverse fetal effects.

An immunotoxicity study (required in accordance with the 2007 revised 40CFR Part 158 

Toxicology Data requirements) has not been submitted for triallate. The existing sub-chronic and 

chronic studies did not indicate that the immune system will be affected by triallate based on 

hematology, lymphoid organ weights, and histopathology measurements. The HASPOC 

recommended waiving the immunotoxicity study based on a weight of evidence approach (TXR# 

0056861). 

Two acute dietary endpoints were selected for triallate. For females of childbearing age (females

13-50, the acute population adjusted dose (aPAD) is derived from a No Observed Adverse Effect 

Level (NOAEL) of 5 mg/kg/day for increased skeletal variations in the rabbit developmental 

study. For the general population, the aPAD is based on a NOAEL of 60 mg/kg/day for altered 

motor activity and changes in functional observation battery (FOB) in the rat acute neurotoxicity 

study. 

The chronic population adjusted dose (cPAD) for the chronic dietary assessment is derived from 

the NOAEL of 2.5 mg/kg/day with a LOAEL of 12.5 mg/kg/day based on decreased survival and 

mean body weights, and increased adrenal weights in the chronic rat study. A total uncertainty 

factor (UF) of 100 (10x for interspecies extrapolation and 10x for intraspecies variation) is 

applied to the NOAELs.

Endpoints for dermal and inhalation exposure were also based on increased fetal skeletal 

variations observed at the LOAEL of15 mg/kg/day with an oral NOAEL of 5 mg/kg/day for 

developmental effects in the rabbit study. A dermal absorption factor of 1% was used in this 

assessment and inhalation toxicity is assumed to be equivalent to oral toxicity. Since both dermal 

and inhalation endpoints were based on the same toxicological effects, these route- specific 

margins of exposure (MOEs) were combined into a total MOE.

An MOE of 100 (10x for interspecies extrapolation and 10x for intraspecies variation) is 

adequate for short- and intermediate-term dermal and inhalation occupational risk assessments

(there are no non-occupational uses of triallate). 

See Attachments 2 and 3 for a summary of the most recent toxicological endpoints and points of 

departure (PODs) for use in triallate risk assessments, available toxicity studies, and the toxicity 

profile.

Conclusion: The toxicology database for triallate is complete. HED will re-evaluate the toxicity 

endpoints, points of departure (PoDs) and uncertainty and other factors during registration 

review.

Dietary Exposure

Food Exposure
Page 7 of 24

Triallate is an herbicide active ingredient in the class of thiocarbamates. The HED Metabolism 

Assessment Review Committee has determined that triallate and the TCPSA metabolite should 

be regulated and assessed for dietary exposure (L. Cheng memo of 6/22/98). A tolerance of 0.3 

ppm is established under 40 CFR §180.314(a) for residues of triallate and its metabolite TCPSA 

in/on Bermuda grass hay. Tolerances with regional registrations are also established under 40 

CFR §180.314(c) for residues of triallate and its metabolite TCPSA in/on barley (grain, hay & 

straw), sugar beets (roots, tops & dried pulp), peas (dry, succulent, field hay & vines), and wheat 

(grain, forage, hay and straw). The tolerances on these RACs range from 0.05 ppm for barley 

and wheat grain to 1.0 ppm for barley, pea and wheat hay. There are no tolerances established 

for livestock commodities because there is no secondary transfer of triallate residues to livestock. 

Acute and chronic dietary risk assessments were most recently performed for triallate and the 

TCPSA metabolite using the Dietary Exposure Evaluation Model (DEEM-FCID) Version 2.03 

(D351895, T. Goodlow, 12/09/2008). This model uses food consumption data from the U.S. 

Department of Agriculture’s Continuing Survey’s of Food Intakes by Individuals (CSFII) from 

1994-1996 and 1998. It was performed to support the use of triallate on Bermuda grass grown 

for seed and hay. These acute and chronic analyses were conservative using field trial data, 

empirical processing factors, 100% crop treated values for all commodities, and estimated 

drinking water concentrations (EDWCs). The calculated acute exposure to food and water 

resulted in an estimated risk equivalent to <1% of the acute population adjusted dose (aPAD) at 

the 95th percentile for all population subgroups. Chronic dietary risk calculated from exposures 

to food and water resulted in an estimated risk equivalent to <1% of the chronic population 

adjusted dose (cPAD) for all population subgroups as well. 

Triallate is concluded to be a possible human carcinogen; therefore, a cancer dietary risk 

assessment was performed which determined a cancer risk estimate of 3.0 x 10-7for the general 

U.S. population.

Drinking Water Exposures

Drinking water exposures can potentially occur through run-off resulting from the applications of 

the herbicide triallate made to control weeds. To assess this potential exposure, the 

Environmental Fate and Effects Division (EFED) most recently modeled values for ground water 

as well as surface water in support of its use on Bermuda grass grown for seed and hay 

(D358774, 11/20/2008, F.Khan). The EDWCs for the use on Bermuda grass did not exceed the 

values previously determined for wheat grown in North Dakota reported in the 2001 Triallate 

Reregistration Eligibility Decision (RED) document. Therefore, the EDWCs determined for the 

wheat scenario were used for assessment. For the wheat scenario, ground water EDWCs were 

estimated using the SCI-GROW (Tier I) computer model. Model simulations indicate that the 

maximum total triallate residue (triallate + TCPSA) concentrations in ground water are not likely 

to exceed 0.21 ppb. Surface drinking water concentrations were estimated using the 

PRZM/EXAMS (Tier II) computer model with the Index Reservoir and Percent Crop Area. Tier 

II PRZM-EXAMS modeling predicts that the maximum total triallate residue (triallate + 

TCPSA) concentration in surface water is not likely to exceed 9.45 ppb for peak (acute) 

concentration and 1.26 ppb for 36-year annual mean (chronic: cancer and non-cancer) 

concentrations. The triallate label states that this product is to be incorporated into soil. Surface 
Page 8 of 24

water EDWCs were modeled with and without incorporation, and the highest value of the two 

were used for the dietary assessment. 

Data Requirements 

The 2001 RED for triallate required that a barley processing study and a field accumulation 

rotational crop study must be provided. The barley processing study has since been waived and 

the data from wheat processing studies may be translated to barley (D278935, S. Knizner, 

11/26/2001). A rotational crop study was submitted in 2004 (MRID No. 46296301) and is 

undergoing review to determine if this fulfills the data requirement. As such, the residue 

chemistry database for triallate is otherwise complete and there are no outstanding data 

requirements for this chemical. 

Conclusions: Currently there are no acute or chronic (food and drinking water) dietary risk 

estimates which are of concern for triallate and its metabolite. Updated dietary exposure 

assessments for triallate may be necessary under registration review if the toxicological PoDs or 

uncertainty factors/safety factors (UFs/SFs) change, or there are significant changes in the 

EDWCs.

Residential (Non-Occupational) Exposure

There are no residential uses for triallate nor are there any occupational uses resulting in 

residential post-application exposure, at this time. 

Residential Bystander Exposures

Residential bystander exposures resulting from off-site transport (e.g., spray drift or 

volatilization) may occur as a result of agricultural applications of triallate. The potential for 

spray drift will be quantitatively evaluated for each pesticide during the Registration Review 

process which ensures that all uses for that pesticide will be considered concurrently. The 

approach is outlined in the revised (2012) Standard Operating Procedures for Residential Risk 

Assessment (SOPs) – Residential Exposure Assessment Standard Operating Procedures Addenda 

1: Consideration of Spray Drift. This document outlines the quantification of indirect nonoccupational exposure to drift. In terms of volatilization, the agency has developed a 

Volatilization Screening Tool and a subsequent Volatilization Screening Analysis 

(http://www.regulations.gov/#!docketDetail;D=EPA-HQ-OPP-2014-0219). During Registration 

Review, the agency will utilize this analysis to determine if data (i.e., flux studies, route-specific 

inhalation toxicological studies) or further analysis is required for triallate.

Aggregate Risk Assessment

In accordance with the Food Quality Protection Act (FQPA), HED must consider and aggregate 

pesticide exposures and risks from three major sources: food, drinking water, and residential 

exposures. The acute and chronic aggregate risk assessments for triallate included food and 

drinking water only (there are no registered residential uses). 
Page 9 of 24

Acute

The 2008 acute aggregate risk assessment included exposure to triallate and TCPSA residues in 

food and water. The analysis used field trial data, empirical processing factors and 100 percent 

crop treated (%CT) for all commodities. Estimated drinking water concentrations from the 

Environmental Fate and Effects Division were also included. Acute dietary risk estimates for 

food alone and food and drinking water at the 95th percentile of exposure are below HED’s level 

of concern with exposures utilizing <1% of the aPAD.

Chronic

The 2008 chronic aggregate risk assessment (cancer and non-cancer) included exposure to 

triallate and TCPSA residues in food and water. Both the cancer and non-cancer analyses 

utilized field trial data, empirical processing factors, 100% CT, and incorporated EDWC values. 

The assessments resulted in dietary risk estimates for food alone and food and drinking water 

that are below the HED’s level of concern for chronic dietary exposure. For non-cancer 

exposure, the highest exposure and risk estimates were for all infants (<1 year), with a cPAD of 

<1% including food and drinking water. For the cancer assessment, the estimated dietary 

exposure for the general U.S. population corresponded to a cancer risk of 3 x 10-7for food and 

drinking water.

Conclusions: During registration review, updated aggregate assessments may be conducted as 

required to include any significant change that might occur for toxicological PODs, FQPA and 

uncertainty factors, dietary exposure estimates, or EDWCs. 

Occupational Exposure

Triallate is registered for agricultural use on Bermuda grass (grown for seed or hay), dry beans 

and peas, green peas, lentils, barley, triticale, wheat, and sugar beets. There is potential for 

occupational handler and post-application exposure.

Occupational Handler Exposure

Triallate can be applied with a groundboom, tractor- drawn spreader, or enclosed fixed wing

aircraft, at a rate of up to 1.5 lbs active ingredient (a.i.) per acre for liquids and granules. Based 

on the handler activity use pattern the duration of exposure is only short-term and intermediateterm for occupational handlers. This is based on the fact that there are different planting periods 

of the registered crops for triallate. Based on the current use pattern (maximum application rate 

of 1.5 lb (a.i.) /A per year) and handler activities, long-term dermal exposure is not anticipated. 

The PPE on the emulsifiable concentrate product labels is baseline protection for all handlers; 

mixer/loaders are also required to wear chemical-resistant gloves. The PPE on the granular 

product labels is baseline for all handlers; loaders must also wear dust/mist respirators. 

The RED assessed all occupational handler scenarios except for the use on Bermuda grass, 

which was assessed in 2008. For occupational handlers, MOE(s) above 100 do not exceed 
Page 10 of 24

HED's level of concern. All short- and intermediate-term combined dermal and inhalation 

occupational exposure risk estimates for granular and liquid formulations did not exceed HED's 

level of concern at the baseline protection and enclosed fixed wing-aircraft scenarios except for 

two mixing/loading liquid scenarios. However with additional PPE (gloves) to minimize dermal 

exposures for these two scenarios, exposure risk estimates were not of concern.

An assessment was conducted for the carcinogenic risk estimates associated with triallate 

following exposures to occupational handlers (private and commercial; mixers, loaders and 

applicators). Based on the RED and 2008 risk assessments, all occupational handler cancer risk 

estimates with label required PPE do not exceed 5 x 10-5. 

Recommended unit exposures for occupational handler assessments have generally been derived 

only from the Pesticide Handlers Exposure Database (PHED). However, recently both the 

Outdoor Residential Exposure Task Force (ORETF) and the Agricultural Handler Exposure Task 

Force (AHETF) have produced pesticide handler exposure monitoring data that the Agency is 

using in place of PHED (http://www.epa.gov/pesticides/science/handler-exposure-data.html). As 

more reliable data become available, the Agency will continue to replace existing data. 

Reviewers should incorporate new exposure monitoring data, as necessary, during registration 

review.

Conclusions: An updated occupational handler assessment may be required under registration 

review if warranted by any significant changes in exposure assessment methodology, 

toxicological PODs or uncertainty factors.

Occupational Post-application Exposure

No DFR (Dislodgeable Foliar Residue) data or exposure monitoring data were submitted for 

triallate. However, HED believes that the potential for post-application worker exposure for all 

uses except Bermuda grass is low, provided the 12 hour restricted entry interval is observed. 

There is low potential for exposure due to the timing of applications. Triallate is applied to the 

soil and/or soil incorporated pre-emergence for wheat, barley, peas, lentils, and sugar beets. This 

is well before the plants are mature, which likely mitigates the potential for post-application 

exposure due to contact with treated foliage. Significant exposure to triallate during mechanical 

planting, harvesting, or any other late season activities, is not likely since triallate is applied preemergent (per Exposure Scientific Advisory Committee (SAC) policy #8). Also significant 

exposure to triallate during scouting, or while handling or coming in contact with treated soil is 

minimal and would not exceed HED's level of concern. Therefore, HED does not require that 

any postapplication exposure data be generated to support the reregistration of triallate.

An exposure assessment was previously completed for exposure to triallate for workers entering 

treated Bermuda grass fields (D351897). Occupational postapplication dermal exposure may 

occur after use of triallate on Bermuda grass grown for seed or hay as triallate can be applied to 

established stands, the REI is 12 hours, and irrigation is not required until 7 days after 

application to incorporate triallate. Based on the previous assessment, the MOE was 2,200 for 

post-application activities associated with Bermuda grass. Cancer risk estimates were < 7 x 10-6 

for post-application workers. Based on a screen using updated exposure assessment policy using 
Page 11 of 24

forage crop assessment as surrogate for Bermuda grass, DFR data are not required as MOEs are 

greater than 2X the LOC.

In accordance with 40CFR158, DFR data are required for all occupational (e.g., crop, nursery, 

greenhouse use sites) or residential (e.g., ornamental and vegetable gardens, pick your own 

farms, retail tree farms) uses that could result in post-application exposure to foliage. In the 

absence of chemical-specific DFR data, EPA uses default values. The 2012 Standard Operating 

Procedures for Residential Pesticide Exposure Assessment includes an analysis of a number of 

DFR studies, which resulted in the selection of a revised default values for the fraction of the 

application rate available for transfer after a foliar application (FAR). These values are based on 

an analysis of 19 DFR studies. Since that time, the Agricultural Re-entry Task Force has 

submitted information (MRID 49299201) that corrects an application rate error made in the 

original submission of “ARF039 – Determination of Dermal and Inhalation Exposure to Reentry 

Workers During Chrysanthemum Pinching in a Greenhouse” (EPA MRID 45344501). As a 

result, the range of FAR values was revised from 2% - 89% to 2% - 47%. In the data, a large 

range of transferability is observed and this variability can potentially be attributable to many 

factors such as active ingredient; formulation; field conditions in the studies; weather conditions 

(e.g., humidity); or many other difficult to quantify factors. Although witnessed across multiple 

chemicals, this range in FAR values is not expected when considering DFR data for a single 

chemical. At this time, the ARTF submission did not alter the selection of 25% as the 

reasonable, high-end default value. Because DFR data are not available for triallate, EPA is 

using the default value of 25%. Although there may be a small degree of uncertainty in the use 

of the default DFR value for triallate (i.e., there is a small chance that the FAR value may exceed 

the applicable default value), it is likely that the health-protective aspects of EPA’s occupational

post-application assessment methodology will more than compensate for this potential 

uncertainty. For example, when assessing residential and occupational post-application 

exposure to gardens and ornamentals, EPA assumes the following: exposures occur to zero-day 

(i.e., day of application ) residues every day of the assessed exposure duration (i.e., EPA assumes 

that no dissipation or degradation occurs, it doesn’t rain, etc); individuals perform the same postapplication activities performed in the transfer coefficient study day after day (e.g., weeding, 

harvesting, pruning, etc.); and individuals engage in these post-application activities for a highend amount of time every day (represented by data reflecting time spent gardening based on 

survey data).

Given the conservatisms discussed above and the potential compounding nature of these 

conservatisms, EPA is able to rely upon the calculated exposure estimates with confidence that 

exposure is not being underestimated. 

Since the highest estimated occupational post-application exposure using default DFR values for 

triallate is minimal in comparison to the level of concern (i.e., the calculated MOE is greater than 

2 times higher than the level of concern, MOE = 540 compared to the LOC of 100); EPA is 

waiving the 40CFR DFR data requirement. In this instance, it is unlikely that chemical-specific 

DFR data would be needed to further refine exposure assessments or would add appreciably to 

our overall understanding of the availability of dislodgeable foliar pesticide residues for triallate. 
Page 12 of 24

Recommended transfer coefficients for occupational post-application assessments are derived 

from Agricultural Reentry Task Force (ARTF) exposure monitoring studies 

(http://www.epa.gov/pesticides/science/post-app-exposure-data.html). These transfer 

coefficients have been updated in 2012 based on a reanalysis and submission of new monitoring 

data. Reviewers should incorporate new exposure monitoring data, as necessary, during 

registration review.

The Worker Protection Standard (WPS) Restricted Entry Interval (REI) for triallate is 12 hours.

Conclusions: An updated occupational post-application assessment may be required under 

registration review if warranted by any significant changes in exposure assessment methodology. 

No chemical-specific DFR or TTR data are required for triallate.

Public Health and Pesticide Epidemiology Data

HED has evaluated the available incident data1and concludes that there does not appear to be a 

concern at this time that would warrant further investigation, since there were no incidents 

involving triallate reported to either IDS or SENSOR-Pesticides. The Agency will continue to 

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

included in the risk assessment.

Tolerance Assessment and International Harmonization

Permanent tolerances are established under 40 CFR §180.314 for the registered uses of triallate 

on raw agricultural commodities. A spreadsheet summarizing the international residue limits 

established for triallate and its metabolite TCPSA is presented in Attachment 4. There are no 

MRLs established for the residues of triallate by Codex or Mexico. Canada has established 

MRLs on triallate for a number of commodities which are harmonized with those tolerances set 

by the U.S. As such, there are no international harmonization issues which are in difference with 

the tolerances established for the herbicide triallate. 

As per the HED memo on tolerance expressions (S. Knizner, 2009, Interim Guidance on 

Tolerance Expressions), the tolerance expressions for triallate should be revised as follows:

 

(a) General. Tolerance are established for residues of the herbicide triallate, including its 

metabolites and degradates, in or on the commodities in the table below. Compliance 

with the tolerance levels specified below is to be determined by measuring only the sum 

of triallate, S-(2,3,3-trichloro-2-propen-1-yl) N,N-bis(1-methylethyl)carbamothioate, and 

its metabolite 2,3,3-trichloroprop-2-enesulfonic acid (TCPSA), calculated as the 

stoichiometric equivalent of triallate, in or on the commodity.

(c) Tolerances with regional registrations. Tolerances with a regional registration, as 

defined in 180.1(l) are established for residues of the herbicide triallate, including its 

metabolites and degradates, in or on the commodities in the table below. Compliance 

 

1 Triallate: Tier I Review of Human Incidents. E. Evans, 5/8/14. D420141.
Page 13 of 24

with the tolerance levels specified below is to be determined by measuring only the sum 

of triallate, S-(2,3,3-trichloro-2-propen-1-yl) N,N-bis(1-methylethyl)carbamothioate, and 

its metabolite 2,3,3-trichloroprop-2-enesulfonic acid (TCPSA), calculated as the 

stoichiometric equivalent of triallate, in or on the commodity.

International or Intergovernmental Work Sharing

HED is not currently involved in any joint international review projects that involve the active 

ingredient, triallate. Additionally, HED is unaware of any ongoing international assessments for 

triallate. 

Cumulative 

The FQPA requires the Agency to consider the cumulative risks of chemicals sharing a common 

mechanism of toxicity. Triallate is a member of the thiocarbamate class of pesticides. The 

Agency has determined that the thiocarbamate pesticides should not undergo cumulative 

assessments since chemicals in the group do not act the same way in the body. In late 2001 and 

early 2002, EPA provided an opportunity for the public to comment on the Agency’s common 

mechanism determinations for the thiocarbamates, which also belong to the carbamate group of 

pesticides. EPA determined that the thiocarbamates do not share a common mechanism of 

toxicity2. Therefore, a cumulative risk assessment has not been performed.

Human Studies 

There are no triallate-specific human studies that require an ethics review at this time.

Data Requirements

The following data deficiencies were identified for triallate:

Toxicology: None

Residue Chemistry: 

 Submittal of Analytical Reference Standards

 

2 http://www.epa.gov/oppsrrd1/cumulative/
Page 14 of 24

o The current stock of TCPSA standards available in the EPA National Pesticide 

Standards Repository has expired (personal communication with Theresa Cole, 

BEAD, 03/28/2014). Analytical reference standards of TCPSA must be provided 

with an updated certificate of analysis (COA) or new materials sent to the 

Repository as soon as possible. The reference standards should be sent to the 

Analytical Chemistry Lab, which is located at Fort Meade, to the attention of 

either Theresa Cole or Thuy Nguyen at the following address:

USEPA

National Pesticide Standards Repository/Analytical Chemistry Branch/OPP

701 Mapes Road

Fort George G. Meade, MD 20755-5350

(Note that the mail will be returned if the extended zip code is not used.)

Occupational and Residential Exposure: None

References

Triallate. PC Code 078802. Outcome of the Metabolism Assessment Review Committee 

Meeting Held on May 14, 1998. L. Cheng, June 22, 1998. No. 012656.

Triallate. Acute, Chronic, and Cancer Aggregate Dietary (Food and Drinking Water) Exposure 

and Risk Assessments for the Section 3 Registration Action on Bermuda Grass. T. Goodlow, 

December 09, 2008. D351895.

Triallate. Revised Drinking Water Exposure Assessment to establish tolerances of triallate and 

its degradate 2,3,3-trichloro-2-propenesulfonic acid (TCPSA) on Bermuda grass grown for seed. 

F. Khan, November 20, 2008. D358774.

Triallate. Wheat Hay/Barley Hay Data Waiver Request. Guideline 860.1500. Chemical 

Number 078802. S. Knizner, November 26, 2001. D278935.

446296301 Moran, S. J. and Beasley, R. K. (2004) Residues of Triallate in Rotational Crop Raw 

Agricultural Commodities Following Application of Far-GO® Herbicide . Report Number MSLI7772. Unpublished study prepared by Monsanto Company. 226 p. 

Triallate: Risk Assessment for Proposed New Use of Triallate as Pre-emergence Herbicide for 

Bermuda grass, Case #824883. A. LaMay, 12/8/08. D351897

Triallate. HED Reregistration Eligibility Document. PC Code: 078802. DP Barcode D260034. 

J. Morales.

Triallate: Tier I Review of Human Incidents. E. Evans, 5/8/14. D420141
Page 15 of 24

Attachment 1. Chemical Identity and Physicochemical Properties of Triallate

Physical and Chemical Properties of Triallate [S-(2,3,3-trichloro-2-propen-1-yl) N,N-bis(1-

methylethyl)carbamothioate]

Table 1. Triallate Nomenclature.

Compound Chemical Structure

Common name Triallate

Company experimental name N/A

IUPAC name S-2,3,3-Trichloroallyl diisopropyl- thiocarbamate

CAS name S-(2,3,3-trichloro-2-propen-1-yl) N,N-bis(1-methylethyl)carbamothioate

CAS # 2303-17-5

End-use product/(EP) Far-GO® Granular Herbicide

Avadex® MicroActiv Herbicide

TCPSA Metabolite Nomenclature.

Compound Chemical Structure

S

Cl

Cl

Cl

O

O

HO

Common name TCPSA

Company experimental name N/A

IUPAC name 2,3,3-Trichloroprop-2-enesulfonic acid

Table 2. Physicochemical Properties of Technical Grade Triallate.

Parameter Value Reference

Melting point/range 29-30°C

Triallate Product Chemistry 

Chapter, D078802, 7/29/99, J. 

Morales. 

Density 1.2600-1.2624 at 35°C 

Water solubility 4 ppm at 25°C

Solvent solubility Soluble in methylene chloride, n-octanol, and 

toluene at >200 g/100 mL

Vapor pressure 1.1 x 10-4 mm Hg at 25oC

Dissociation constant (pKa) Not Provided

Octanol/water partition coefficient 

log (Kow) 

4.54

UV/visible absorption spectrum Not Provided

H3C N

CH3

H3C CH3

O

S

Cl

Cl

Cl
Page 16 of 24

Attachment 2. Acute, Subchronic, and Chronic Toxicity Profile

Acute Toxicity of Technical Triallate

Guideline Study Type (Date) MRID Results Tox. 

Cat.

870.1100 

(§ 81-1)

Acute Oral-Rat

(6/29/98)

44660701 LD50 (males) = 3612 mg/kg

(265-4909 mg/kg)

LD50 (females) = 3455 mg/kg

(2590-4611 mg/kg)

LD50 ( combined) = 3382 mg/kg (2755-4151 

mg/kg)

III

870.1200 

(§ 81-2)

Acute Dermal-Rabbit (1/11/91) 42192001 LD50 > 5000 mg/kg IV

870.1300 

(§ 81-3)

Acute Inhalation-Rat

(9/9/82)

00121856 LC50 > 5.3 mg/L IV

870.2400 

(§ 81-4)

Primary Eye Irritation-Rabbit

(1/22/98)

44591801 Slight eye irritant III

870.2500 

(§ 81-5)

Primary Dermal IrritationRabbit (1/27/98)

44581601 Slight dermal irritant IV

870.2600 

(§ 81-6)

Dermal Sensitization-Guinea 

pig Buehler test (10/7/83)

00132879 Non sensitizer N/A

870.2600 

(§ 81-6)

Dermal Sensitization-Guinea pig 

maximization test (6/6/97)

44308301 Dermal sensitizer N/A

Sub-chronic, Chronic, and Other Toxicity Profiles for Triallate

Guideline Study Type (Date) MRID Results

Subchronic Toxicity

870.3100 

(§ 82-1)

90-Day Feeding- Rat

(8/23/82)

00115639 Systemic NOAEL=100 ppm (5/mg/kg/day)

Systemic LOAEL=500 ppm (25 mg/kg/day) based on 

decreased body weight in males and females, slight

anemia in females (decreased red blood cells,

hematocrit and hemoglobin) and histopathology of the 

kidney in males (tubular epithelial regeneration and 

nephropathy)

870.3200 

(§ 82-2)

21-Day Dermal-Rat

(1/29/90)

41487001 Systemic NOAEL = 500 mg/kg/day

Systemic LOAEL = 3000 mg/kg/day based on body weight

gain decreases, relative kidney and liver weight increases,

increased presence of basophilic tubules of the renal cortex, 

and alphaμ-globulin inclusions in the proximal convoluted 

renal tubules.

Dermal NOAEL<100 mg/kg/day

Dermal LOAEL=100 mg/kg/day based on increased

incidences of acanthotic epidermal thickening.
Page 17 of 24

(§ 82-2) Subchronic Inhalation (6 

hr/day 5 days/week for 7 

weeks)-Rat

(9/27/83)

40072105

00132878

NOAEL < 0.01 mg/L (2.62 mg/kg/day) not established

LOAEL=0.01 mg/L (2.62 mg/kg/day) based on 

histological changes in the kidney (nephropathy and 

tubular epithelial regeneration).

Chronic Toxicity/Carcinogenicity

870.4100 

(§ 83-1)

Chronic Toxicity- Dogs

(10/2/79)

00029455 Systemic NOAEL=1.5 mg/kg/day (1.27 mg/kg/day 

calculated)

Systemic LOAEL=5.0 mg/kg/day (4.25 mg/kg/day 

calculated) based on increased hemosiderin

deposition in the spleen, increased serum alkaline

phosphatase and increased liver weight in females.

870.4100 

(§ 83-1)

Chronic Toxicity- Dogs

(2/4/88)

40730604 Systemic NOAEL=2.5 mg/kg/day

Systemic LOAEL=15.0 mg/kg/day based on increased 

alkaline phosphatase levels at all time intervals in male and 

female dogs.

870.4200 

(§ 83-2)

Chronic Toxicity/ 

Carcinogenicity -Rat 

(7/10/87)

40384701

41116901

NOAEL= 50 ppm (2.5 mg/kg/day).

LOAEL= 250 ppm (12.5 mg/kg/day) based on decreased 

survival (males and females), decreased body weight

(males) and increased adrenal weight (males).

Evidence of carcinogenicity: Renal tubular 

adenomas in male rats.

870.4200 

(§ 83-2)

Chronic Toxicity/ 

Carcinogenicity -Mice 

(10/83)

00132859 NOAEL(males) = 20 ppm (3 mg/kg/day)

LOAEL (males) = 60 ppm (9 mg/kg/day) based on increased 

absolute liver weight, increased incidence of altered foci of 

the liver and hematopoiesis in the spleen.

NOAEL(females) = 250 ppm (37.5 mg/kg/day) 

LOAEL(females) >250 ppm (37.5 mg/kg/day) not established

Evidence of carcinogenicity: Increased incidence of 

hepatocellular carcinomas and hepatocellular adenomas 

(males).

870.4200 

(§ 83-2)

Chronic Toxicity/ 

CarcinogenicityHamster (10/18/84)

00151790

00159797

NOAEL=50 ppm

LOAEL=300 ppm based on decreased triglyceride levels 

(males and females).

No evidence of carcinogenicity

Developmental/Reproductive Toxicity

870.3700 

(§ 83-3)

Developmental Toxicity-Rat

(5/10/82)

00114260

41706906

Maternal NOAEL = 10 mg/kg/day

Maternal LOAEL = 30 mg/kg/day based on decreases in 

body weight gain and food consumption.

Developmental NOAEL = 30 mg/kg/day Developmental

LOAEL = 90 mg/kg/day based on decreased fetal body

weight, external malformations (protruding tongue) and 

skeletal variations.
Page 18 of 24

870.3700 

(§ 83-3)

Developmental ToxicityRabbit

(1/21/82)

00114261

43315001

Maternal NOAEL = 15 mg/kg/day

Maternal LOAEL = 45 mg/kg/day based on clinical 

signs and decreases in body weight gain.

Developmental NOAEL = 5 mg/kg/day Developmental

LOAEL = 15 mg/kg/day based on decreased fetal body

weight and increased skeletal variations.

870.3800 

(§ 83-4)

2-Generation Reproduction

Study-Rat

(10/20/83, 7/11/84)

00144308

00132880

Parental/Systemic NOAEL = 150 ppm (7.5 mg/kg/day) 

Parental/Systemic LOAEL = 600 ppm (30 mg/kg/day) 

based on maternal mortality, increased incidences of 

chronic nephritis, head bobbing, circling movements and 

reduced body weights.

Reproductive/Developmental NOAEL = 150 ppm (7.5 

mg/kg/day).

Reproductive/Developmental LOAEL = 600 ppm (30 

mg/kg/day) based on increased neonatal mortality during 

the F2b litter interval, reduced pup weights at

birth during the F2b litter interval, reduced pup weights in 

late lactation for all litters, reduced pregnancy rate and 

shortened gestation length.

Mutagenicity

870.5100 

(§84-2)

Gene Mutation in Salmonella 

typhimurium

(7/1/77)

00088624 Positive. Triallate induced a mutagenic response in 

Salmonella typhimurium strains TA1535 and TA100 at 

noncytotoxic doses of 0.1 μg/plate and above -S9 activation 

and TA1535, TA98 and TA100 at 0.001

μg/plate and above +S9. In tester strains TA1537 and 

TA1538, there were no appreciable increases in revertant 

colonies or evidence of cytotoxicity at any dose. 

Mutagenesis was confirmed in a repeat test with Salmonella 

typhimurium strain TA1535 at dose levels

of 1, 5, and 10 μg/plate +/- S9 activation.

870.5300 

(§84-2)

Gene Mutation/ In vitro 

mammalian cell assay in 

mouse lymphoma cells 

(8/1/77)

00083644 Negative. Triallate did not induce forward gene 

mutations at the thymidine kinase (TK

+/-

) locus in 

L51784 mouse lymphoma cells at concentrations of

0.005 to 0.04 μl/mL in the absence or presence of 

metabolic activation.

870.5300 

(§84-2)

Gene Mutation/ In vitro 

mammalian cell assay in 

mouse lymphoma cells 

(8/1/77)

41091007 Positive. Triallate induced forward gene mutations at the 

thymidine kinase (TK

+/-

) locus in L51784 mouse lymphoma 

cells. The frequency of gene mutations

was greater than or equal to a two-fold increase and 

occurred at noncytotoxic concentrations of 60 μg/mL

-S9 activation and 21 and 24 μg/mL+S9 activation.

870.5385 

(§84-2)

Cytogenetics/ In vivo

hamster micronucleus assay

(5/7/82)

00114263 Negative. There was no evidence of either a clastogenic or 

aneugenic effect in male and female hamsters fed dietary

concentrations of 0, 600, 2000 or

6000 ppm Triallate at any sacrifice time.

870.5395 

(§84-2)

Cytogenetics/ In vivo mouse 

micronucleus assay (1/15/91, 

10/15/97; Amendment)

44591701 Negative. There was no evidence of either a clastogenic

or aneugenic effect in male and female mice administered 

70, 350, or 700 mg/kg Triallate at any sacrifice time.
Page 19 of 24

870.5550 

(§84-2)

Other Mutagenic Mechanisms/ 

In vitro unscheduled DNA

synthesis in primary rat

hepatocytes (11/14/85)

40730601 Negative. Triallate did not induce a genotoxic effect in 

primary rat hepatocytes at concentrations of 5, 10, 50,

100, 500 and 1000 μg/mL.

870.5550 

(§84-2)

Other Mutagenic Mechanisms/ 

In vivo/In vitro unscheduled 

DNA synthesis in primary rat

hepatocytes (9/20/89, 9/25/89; 

Amendment)

44701001 Negative. There was no evidence that Triallate induced

either a cytotoxic or genotoxic response at any dose (50,

250 or 500 mg/kg) or sacrifice time (92 or 16 hours).

870.5900 

(§84-2)

Other Mutagenic Mechanisms/ 

In vitro sister chromatid 

exchange in Chinese hamster 

ovary cells (9/3/82)

00121859 Positive. Triallate induced significant increases in the 

number of sister chromatid exchanges per cell at 

concentrations of 1.6 x 10

-5 M to 8.1 x 10-5 M -S9

activation and 0.8 x 10

-5 M to 4.0 x 10-5 M +S9

activation after either a two or four hour exposure period, 

respectively. Repeat assays conducted for 30 hours at

concentrations up to 40.4 x 10

-5 M -S9

activation and for 2 hours at concentrations up to 12.1 x 10

-5

M +S9 activation confirmed these findings.

Neurotoxicity

870.6100 

(§ 81-7)

Acute Delayed NeurotoxicityHen

(8/10/83)

00132874

40072104

Systemic NOAEL≺312.5 mg/kg (not established)

Systemic LOAEL=312.5 mg/kg based on acute, reversible 

clinical signs (muscle weakness/paralysis, salivation and 

involuntary neck movement) Triallate did not induce delayed

peripheral neuropathy

870.6200 

(§ 81-8)

Acute Neurotoxicity-Rat

(7/8/93)

42908101 Systemic NOAEL=60 mg/kg

Systemic LOAEL=300 mg/kg based on decreased body

weight gain and alterations in motor activity

870.6200 

(§ 82-7)

Subchronic Neurotoxicity-Rat

(11/17/93)

43021601 Systemic/Neurotoxicity NOAEL=100 ppm (6.38/8.14 

mg/kg/day for males/females) Systemic/Neurotoxicity

LOAEL=500 ppm (32.9/38.9 mg/kg/day for

males/females) based on decreased body, body weight 

gains , food consumption and lesions (nerve fiber 

degeneration) in the central and peripheral nervous 

systems.

870.6200 

(§ 82-7)

Subchronic Neurotoxicity-Rat

(11/3/98)

44694501 Neurotoxic NOAEL= 2000 ppm (achieved dose 134.32 

mg/kg/day)

Neurotoxic LOAEL = 4000 ppm (achieved dose 223.79 

mg/kg/day) based on behavioral effects

(histopathology for axonal degeneration was not 

conducted at this dose level)

At 6000 ppm (295 mg/kg/day) neurohistopathological 

lesions in both the central and peripheral nerves.

Systemic NOAEL = 500 ppm (34.64 mg/kg/day) Systemic

LOAEL = 2000 ppm (achieved dose 134.32

mg/kg/day) was based on decreased body weight and food 

consumption and food efficiency.
Page 20 of 24

870.6300 

(§ 83-6)

Developmental NeurotoxicityRat

(12/2/98)

44710501 Maternal NOAEL = 30 mg/kg/day

Maternal LOAEL = 60 mg/kg/day based on reductions in 

body weight gains and food consumption

Developmental Neurotoxicity NOAEL = 30 mg/kg/day 

Developmental Neurotoxicity LOAEL = 60 mg/kg/day 

based on increased motor activity.

Metabolism

870.7485 

(§ 85-1)

General Metabolism-Rat

(10/6/83, Part I)

00138159 Analysis of whole body elimination in male and female rats

indicated that 85% of the radiolabeled triallate was excreted

within 24 hours of dosing. Most radioactivity was excreted 

in approximately equal amounts (42%) in the urine and feces 

of male rats after 10 days.

Females excreted 51% in urine and 32% in feces after

10 days. Males and females retained about 0.4% of the 

dose in organs and tissues and approximately

2.0% in the remaining carcass. The distribution of

radioactivity in both sexes indicated that the greatest amount

of activity was found in the red blood cells followed by

whole blood, spleen, kidney, liver and lung.
Page 21 of 24

Toxicology Data Requirements

The toxicology data requirements (40 CFR 158.340) for the food uses of triallate are presented below. Use of the new 

guideline numbers does not imply that the new (1998) guideline protocols were used.

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 Sub-chronic (rodent)...............................................

870.3150 Oral Sub-chronic (nonrodent).........................................

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

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

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

yes 

yes 

yes 

CR 

yes

yes 

yes 

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 (non-rodent)........................................

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

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

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

yes 

no 

yes 

yes 

yes

yes 

yes 

yes 

yes 

yes

870.5100 Mutagenicity—Reverse Mutation - bacterial.................

870.5375 Mutagenicity—Chromosomal Aberrations-mammalian

870.5395 Mutagenicity—Mammalian Micronucleus....................

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..............................................................

yes

no 

yes 

yes 

yes

yes

no 

yes 

yes 

yes

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

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

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

yes

no 

yes

yes

no

 yes**

* 7 week inhalation study is available, ** Waived by HASPOC (TXR# 0056861)
Page 22 of 24

Attachment 3. Triallate Toxicological Doses and Endpoints for Risk Assessment

Toxicological Doses and Endpoints for Triallate Human Health Risk Assessments.

Exposure

Scenario

Point of

Departure

Uncertainty/FQPA 

Safety Factors

RfD, PAD, Level 

of Concern for 

Risk Assessment

Study and Toxicological Effects

Acute Dietary

(Females 13-49)

NOAEL=5 

mg/kg/day

UFH = 10X 

UFA = 10X

Total UF = 100X 

FQPA = 1X

acute RfD= 0.05

mg/kg/day

aPAD = Acute RfD

FQPA Factor

aPAD = 0.05 

mg/kg/day

Rabbit Developmental Study

LOAEL= 15 mg/kg/day based on increased skeletal 

variationsin the fetus. The skeletal variations are

presumed to occur after a single exposure (dose) and

thus are appropriate for this (acute) risk assessment. In

addition, skeletal variations (malaligned sternebrae)

were also seen in rat fetuses following in utero exposure

to triallate.

Acute Dietary 

(General US 

Pop.)

NOAEL=60 

mg/kg/day

UFH = 10X

UFA = 10X

Total UF = 100X 

FQPA = 1X

acute RfD= 0.6

mg/kg/day

aPAD = Acute RfD

FQPA factor

aPAD = 0.6 

mg/kg/day

Rat Acute Neurotoxicity Study

LOAEL=300 mg/kg/day based on altered motor activity 

and changes in FOB in the rat acute neurotoxicity study. 

Because of the neurotoxic characteristics of triallate (altered

motor activity observed in both sexes 7 hours after 

treatment at the mid- and high- doses that persisted up to

14 days in high-dose females), this endpoint is considered 

appropriate for assessing risk in the general population.

Chronic Dietary

(all populations)

NOAEL =

2.5 

mg/kg/day

UFH = 10X 

UFA = 10X

Total UF = 100X 

FQPA SF = 1X

Chronic RfD=

0.025 mg/kg/day

cPAD =C. RfD

FQPA SF

cPAD = 0.025 

mg/kg/day

2-year chronic toxicity/carcinogenicity in rats

LOAEL=12.5 mg/kg/day based on decreased survival in 

males and females, decreased mean body weights in males 

and increased adrenal weights in males.

Dermal 

Short-Term 

(1 - 30 days)

IntermediateTerm

(1 - 6 months)

Oral 

NOAEL = 5 

mg/kg/day

UFH = 10X 

UFA = 10X

Total UF = 100X

Dermal Absorption =

1% (of oral absorption)

Occupational

LOC = 100

Rabbit Developmental Study

LOAEL= 15 mg/kg/day based on increased skeletal 

variations in the fetus. The 21-day dermal toxicity study 

was not selected because developmental effects were not 

evaluated in that study.
Page 23 of 24

Toxicological Doses and Endpoints for Triallate Human Health Risk Assessments.

Exposure

Scenario

Point of

Departure

Uncertainty/FQPA 

Safety Factors

RfD, PAD, Level 

of Concern for 

Risk Assessment

Study and Toxicological Effects

Inhalation 

Short-Term 

(1 - 30 days)

IntermediateTerm

(1 - 6 months)

Oral 

NOAEL = 5 

mg/kg/day

UFH = 10X 

UFA = 10X 

UFDB = 1X

Total UF = 100X 

Inhalation toxicity is

assumed to be

equivalent to oral 

toxicity

Occupational

LOC = 100

Rabbit Developmental Study

LOAEL= 15 mg/kg/day based on increased skeletal 

variations in the fetus. The 7-week inhalation study was 

not used because the study was classified supplementary 

due to technical difficulties.

Long-Term 

(Dermal & 

Inhalation)

A dose and endpoint were not selected because of the current use pattern, handler activities and re-entry worker activities. Since

long-term dermal exposure (continuous exposure of greater than 180 days) is not anticipated, a quantitative assessment is not

required.

Cancer (oral, 

dermal, 

inhalation)

Group C chemical – possible human carcinogen - Q1* = 7.17 x 10–2(mg/kg/day)-1in human equivalents [converted from 

animals to humans by use of the (mg/kg body weight)

3⁄4

cross species scaling factor] based on hepatocellular carcinomas 

from a chronic/carcinogenicity study in mice.
Page 24 of 24

Attachment 4. International Residue Limits for Triallate

International Residue Limits 

Triallate (078802; 03/27/14)

Summary of US and International Tolerances and Maximum Residue Limits 

Residue Definition:

US Canada Mexico1 Codex

§180.314 (a) General. Tolerances are 

established for residues of triallate, S-

(2,3,3-trichloro-2-propen-1-yl) N,N-bis(1-

methylethyl)carbamothioate and its 

metabolite 2,3,3-trichloroprop-2-

enesulfonic acid (TCPSA) 

carbamothioic acid, N,Nbis(1-methylethyl)-, S-(2,3,3-

trichloro-2-propen-1-yl) 

ester, including the 

metabolite 2-propene-1-

sulfonic acid, 2,3,3-trichloroNone

Commodity Tolerance (ppm) /Maximum Residue Limit (mg/kg)

US Canada Mexico1 Codex

Bermudagrass, hay 0.3

US 40 CFR §180.314 Canada Mexico1 Codex

Plants: (c) Tolerances with regional 

registrations. Tolerances with a regional 

registration, as defined in 180.1(l),are 

established for residues of the herbicide S-

(2,3,3-trichloro-2-propen-1-yl) N,N-bis(1-

methylethyl)carbamothioate and its 

metabolite 2, 3, 3-trichloroprop-2-

enesulfonic acid (TCPSA) 

Same as above None

Commodity Tolerance (ppm) /Maximum Residue Limit (mg/kg)

US Canada Mexico1 Codex

Barley, grain 0.05 0.05

Barley, hay 1.0

Barley, straw 0.3

Beet, sugar, dried pulp 0.2

Beet, sugar, roots 0.1 0.1

Beet, sugar, tops 0.5

Pea, dry 0.2

Pea, field, hay 1.0

Pea, field, vines 0.5

Pea, succulent 0.2

Wheat, forage 0.5

Wheat, grain 0.05 0.05

Wheat, hay 1.0

Wheat, straw 1.0

Completed: M. Negussie; 04/01/14

1 Mexico adopts US tolerances and/or Codex MRLs for its export purposes.