1

EPA REGISTRATION DIVISION COMPANY NOTICE OF FILING FOR PESTICIDE
PETITIONS PUBLISHED IN THE FEDERAL REGISTER

EPA Registration Division contact: Kable Bo Davis (703)306

- 0415

Dow AgroSciences LLC

4F8279

EPA has received a pesticide petition (4F8279) from Dow AgroSciences LLC, 9330 Zionsville Road, Indianapolis, Indiana 46268

, proposing, pursuant to section 408(d) of the Federal Food, Drug, and Cosmetic Act (FFDCA), 21 U.S.C. 346 a(d), to amend 40 CFR part 180. 417 by establishing a tolerance for residues of triclopyr choline salt as triclopyr

, [(3,5,6

- trichloro

- 2

- pyridinyl)oxy] acetic acid, including its metabolites and degradates, in or on the raw agricultural commodit y listed in 40CFR §180.417. EPA has determined that the petition contains data or information regarding the el ements set forth
in section 408 (d)(2) of FDDCA; however, EPA has not fully evaluated the sufficiency of
the submitted data at this time or whether the data supports granting of the petition. Additional data may be needed before EPA rules on the petition.

A. Residue Chemistry

1. Plant metabolism

. The nature of residues is adequately understood and analytical methods are available for the determination of triclopyr in milk and
commodities . EPA has established that the qualitative nature of the residue is adequately
understood based on two studies w ith [14C] triclopyr on grass. Nature of residue studies had shown that majority of the total radioactive residue was triclopyr. No significant amounts of the metabolites 3,5,6

- tr i cihloro

- 2

- pyridinol and 2

- methoxy

- 3,5,6

- trichloropyridine were detected. T he Agency’s HED Metabolism Committee has concluded that the residue to be regulated in grass is triclopyr

.

2. Analytical method. Adequate methodology is available for the enforcement of tolerances for triclopyr residues of concern. Gas chromatography m ethods are available for the determination of triclopyr residues of concern. Residues of triclopyr, 3,5,6

- trichloro

- 2

- pyridinol, and 2

- methoxy

- 3,5,6

- trichloropyridine can be separately
determined

.

3. Magnitude of residues

. Magnitudes of residue studies (MOR) on grass were conducted in 1987, 1976, and 1974 and had been previously submitted. All samples were analyzed for triclopyr using method ACR 77.4. Brief summaries of the MOR studies are
as follows:

The 1987 MOR study was conducted at 11 sites locat ed in 10 different states across the United States (3). XRM

- 4714 formulation (4 lb ae/gal), containing triclopyr as butoxyethyl ester, was applied on actively growing grass as an aqueous diluted ground broadcast spray at a single nominal application rate of 2.0, 4.0, or 6.0 lb ae/A. Grass2

forage and hay were collected at different sampling intervals of 0

- 28 days after application. Grass forage samples were frozen after collection while hay samples were dried before freezing.

The 1976 MOR study was conducted at 3 sites using XRM

- 4021 formulation (4 lb ae/gal) containing triclopyr as butoxyethyl ester (2). XRM

- 4021 was applied as an aqueous diluted spray at a single nominal rate of 1.5 lb ae/A, either as ground (NY and
OR sites ) or aerial (MO site) application. Grass forage samples were collected at different sampling intervals of 0

- 365 days after application and were frozen after
collection.

The 1974 MOR study was conducted at 7 sites located in 6 different states across the United States (1). All 7 sites received ground application and one site received an aerial application, in addition. XRM

- 3724 formulation (3 lb ae/gal), containing tricl opyr as triethyamine salt, was applied on actively growing grass as an aqueous diluted spray at a single nominal application rate of 1.5 lb ae/A. Grass forage samples were collected at different sampling intervals of 0

- 365 days after application and were frozen after
collection.

B. Toxicological Profile

1. Acute toxicity. Acute toxicity studies were performed with triclopyr acid, triclopyr

- TEA

, and triclopyr

- BEE.

i. For triclopyr acid, the acute oral LD50 was 729 mg/kg for males and 630 mg/kg
for fem ales; while acute dermal LD50 was >2000 mg/kg.

ii. For triclopyr

- TEA, the acute oral LD50 was 1847 mg/kg for males and females; the acute dermal LD50 was >2000 mg/kg; the acute inhalation LC50 was >2.6 mg/L; it was corrosive to eyes, not irritating to ski n but was a skin sensitiz er.

iii. For triclopyr

- BEE, the acute oral LD50 was 803 mg/kg for males and females; the acute dermal LD50 was >2000 mg/kg; the acute inhalation LC50 was >4.8 mg/L; it was minimal irritation to eyes, not irritating to skin but was a skin sensitiz er.

The developmental NOAEL of 100 mg/kg/day from a rat developmental study with triclopyr BEE was recommended for the acute dietary risk assessment for general population. This NOAEL was selected based on the toxicity observed at the nex t highest dose (lowest effect level) of 300 mg/kg/day in which mortality, clinical signs, decreased body weight gains, decreased food consumption, increased water consumption, and increased relative kidney and liver weights were recorded. However, the refe rence dose for acute dietary risk assessment for females (13

- 50 years old) is based on a 2

- generation reproductive toxicity study with triclopyr acid in rats with a NOAEL of 5 mg/kg/day and uncertainty factor of 100. The NOAEL was selected based on the inc reased incidence of F2 pup with exencephaly and ablepharia at the next dose level of 25 mg/kg/day. Thus, the population sub

- group of particular interest that would be evaluated in the acute exposure3

assessment are females (13

- 50 years old).

2. Genotoxict

y.

i. Triclopyr acid was negative (non

- mutagenic) in an Ames assay with and without hepatic enzyme activation. It was also negative in a rec

- assay in B. subtilis, in
host

- mediated assay at doses up to 70 mg/kg in mice, in cytogenetic assay for chromosomal aberration at doses up to 70 mg/kg administrated singly or for 5 days to

rats. Triclopyr acid did not produce any evidence of unscheduled DNA synthesis, as determined by radioactive tracer procedures (nuclear silver grain counts), in rat primar y hepatocyte cultures exposed up to cytotoxic levels. It was negative for the dominant lethal mutagenic effect in treated male rats which were fed for 9 consecutive weeks at doses up to 70 mg/kg/day and mated to virgin females. Triclopyr acid was negative for the dominant lethal mutagenic effect in treated male rats at doses up to 70 mg/kg/day given by oral intubation followed by mating to 2 untreated females per week for 7 weeks.

ii. Triclopyr

- BEE was non

- mutagenic, in an Ames assay with and without hepat ic enzyme activation, was not clastogenic in mouse micronucleus test up to 600 mg/kg (HDT) and did not cause DNA damage or inducible repair in the rat hepatocyte unscheduled DNA synthesis. On the basis of the results from this battery of tests, it is
concl uded that, triclopyr is not mutagenic or genotoxic.

3. Reproductive and developmental toxicity

.

i . Developmental toxicity in the rat with triclopyr acid, the maternal NOAEL was <50 mg/kg/day and maternal LOAEL was 50 mg/kg/day based on increased clini cal signs. The developmental NOAEL was 100 mg/kg/day and developmental LOAEL was 200 mg/kg/day based on increased incidence of fetuses and litters with retarded ossification of skull bones, and two litters (one fetus per litter) with cleft palate and brachycephaly.

ii . Developmental toxicity in the rat with triclopyr

- BEE, the maternal NOAEL was 100 mg/kg/day and maternal LOAEL was 300 mg/kg/day based on mortality, clinical signs, necropsy findings, decreased body weight gains, decreased food consumption, increased wate r consumption, and increased relative kidney and liver weight. The developmental NOAEL was 100 mg/kg/day and developmental LOAEL was 300 mg/kg/day based on increased incidence of hydrocephalus, cleft palate, microphthalmia/anophthalmia, retinal folds, thin diaphragm/protrusion of the liver, decreased fetal weight and visceral and skeletal anomalies and variants.

ii i . Developmental toxicity in the rabbit with triclopyr

- BEE, the maternal NOAEL was 30 mg/kg/day and maternal LOAEL was 100 mg/kg/day based on mo rtality. The developmental NOAEL was 30 mg/kg/day and developmental LOAEL was 100 mg/kg/day based on decreased total live fetuses and increased total fetal deaths, as well
as increased fetal and/or litter incidence of skeletal anomalies and variants.4

iv

. Developmental toxicity in the rat with triclopyr

- TEA, the maternal NOAEL was 100 mg/kg/day and maternal LOAEL was 300 mg/kg/day based on mortality. The developmental NOAEL was 100 mg/kg/day and developmental LOAEL was 300 mg/kg/day based on decreased fetal weight, increased fetal and litter incidence of skeletal anomalies, increased fetal incidence of unossified sternebrae.

v . Developmental toxicity in the rabbit with triclopyr

- TEA, the maternal NOAEL was 30 mg/kg/day and maternal LOAEL was 100 mg/kg/day b ased on mortality, abortions, decreased body weight gain, decreased food efficiency, increased liver and kidney weight. The developmental NOAEL was 30 mg/kg/day and developmental LOAEL was 100 mg/kg/day based on decreased live fetuses and increased embryon ic
deaths due to abortions.

v i. Two

- generation reproduction toxicity study in rats, the parental/systemic NOAEL was 5 mg/kg/day in males and in females and parental/systemic LOAEL was 25 mg/kg/day in males and females based on increased incidence of proxi mal tubular degeneration in male and female P1 and P2 rats. The reproductive/offspring NOAEL was 5 mg/kg/day in males and females and reproductive/offspring LOAEL was 25 based on increased incidence of F2 pups with exencephaly and ablepharia.

4. Subchron ic toxicity.

i. In a 90

- day oral study in rats with triclopyr acid, the NOAEL was 5 mg/kg/day in males and females, and LOAEL was 20 mg/kg/day in males and females based on degeneration of the proximal tubules of the kidneys.

ii. In a 90

- day oral study in rats with triclopyr

- BEE, the NOAEL was 7 mg/kg/day in males and < 7 mg/kg/day in females, and LOAEL was 28 mg/kg/day in males, 7 mg/kg/day based on increased relative kidney weight (M) and decreased red blood cell content, hemoglobin content, and packe d cell volume (F). Degeneration of the proximal tubules of the kidneys was seen in males at 70 and 350 mg/kg/day and females at 350 mg/kg/day highest dose tested (HDT).

i ii. In a 183

- day oral study in dogs with triclopyr acid, the NOAEL was ≤2.5 mg/kg/day (HDT) in males and females, and LOAEL was >2.5 mg/kg/day in males and females based on toxicologically non

- significant decreased rate of phenolsulfothalein (PSP) due to competition between triclopyr and PSP for renal excretion.

i v

. In a 3

- week dermal study on rabbits with triclopyr

- BEE, the NOAEL was 1000 mg/kg/day (males and females), and LOAEL was >1000 mg/kg/day based on decreased alkaline phosphatase in both sexes and increased absolute and relative liver weight in males were considered marginal an d not of toxicological significance.

v. As part of the separate ongoing tolerance action with triclopyr in Milk and Milk Fat to support adding dairies as a use site to triclopyr technical and end use labels (OPP
Decision Number: D

- 488479 and D

- 488485) a w eight of evidence waiver request was5

submitt ed for the subchronic inhalation study (MRID# 49306301). The conclusion of the waiver, based on kinetic and metabolism considerations, existing oral studies for triclopyr appear to be adequate to establish point of departure for the subchronic inhalation toxicity endpoints via route

- to

- route extrapolation; in fact it is highly unlikely that the conduct of a new subchronic inhalation study would have any impact on the toxicology end

- points
used for risk assessment ; Animal welfare concern, with particular regards to the acute eye irritation/corrosion may be raised for a repeated a dministration regimen by the inhalatory route and should be considered. From an exposure stem point, the physicochemical properties of th e active indicate a very low potential of exposure from volatilization of the chemical after sprays have settled. The available human exposure data (together with the use pattern for this active ingredient) confirm that that the potential for human

exposur e to triclopyr via inhalatory route is in fact very low and well below the
established reference doses

5. Chronic toxicity

.

i. In a 228

- day feeding study in dogs with triclopyr acid, the NOAEL was 10 mg/kg/day in males and females, and LOAEL was 20 mg /kg/day in males and females based on decreased body weight gain (in males), decreased hematological parameters (in males), changes in clinical chemistry (in both sexes), and liver histopathology (in both sexes).

ii. In a 1

- year feeding study in dogs with triclopyr acid, the NOAEL was ≤5 mg/kg/day in males and females, and LOAEL was >5 mg/kg/day in males and females based on changes in clinical chemistry which are due not to toxicity, but a physiologic response of the dog based on limited ability of the do g to excrete organic acids at higher plasma concentrations.

iii. In a 2

- year rat chronic / carcinogenicity study with triclopyr acid the NOAEL was 12 mg/kg/day in males, ≤ 36 mg/kg/day in females, and LOAEL was 36 in males, >36 mg/kg/day in females based on marginal increases in proximal tubular degeneration at 6 months. Increase in adrenal gland pheochromocytoma in males and significant trend (<0.05) for mammary gland adenocarcinoma in females.

iv. In 22

- months mouse chronic / carcinogenicity study with triclopyr acid the
NOAEL was 84 mg/kg/day in males, 109.5 mg/kg/day in females , and LOAEL was 143 mg/kg/day in males, 135 mg/kg/day in females based on decreased weight gain

. No evidence of carcinogenicity in males, but females had a significant trend (< 0.05) for mammary gland adenocarcinoma.

EPA has established the reference dose (RfD) for triclopyr at 0.05 mg/kg/day for
chronic risk assessment. The RfD is based on a 2

- generation reproductive toxicity study with triclopyr acid in rats with a NOAEL of 5 mg/kg/day and uncertainty factor of 100. The NOAEL was selected based on the increased incidence of proximal tubular degeneration in some P1 and P2 parents of both sexes at the next dose level of 25 mg/kg/day.6

6. Animal metabolism. Disposition and metabol ism of 14C

- triclopyr in rats demonstrated that triclopyr was well absorbed after oral administration. Excretion was relatively rapid with a majority of radioactivity eliminated in the urine by 24 hours. At the high dose of 60 mg/kg, urinary elimination of 14C

- triclopyr was decreased due to apparent saturation of renal elimination mechanisms. Fecal elimination of 14C

- triclopyr was a minor route of excretion, as was elimination via exhaled air. Un

- metabolized parent chemical represented >90% of urinary radi oactivity, with the remainder accounted for by the metabolite 3,5,6

- trichloro

- 2

- pyridinol (3,5,6

- TCP), and possible glucuranide and/or sulfate conjugates of 3,5,6

- TCP. Plasma elimination following intravenous
administration of 14C

- triclopyr was consistent with a one

- compartment model with an
elimination half

- life of 3.6 hour and zero

- order kinetics from 0

- 12 hours at the 60 mg/kg
dose.

7. Metabolite toxicology. In animal metabolism studies, <10% 3,5,6

- trichloro

- 2

- pyridinol (TCP) was found as a significan t metabolite. Toxicity of TCP was studies in a toxicity package of studies viz. acute, sub

- chronic, genotoxicity, developmental toxicity studies revealed that the TCP has similar toxicity as of parent molecule, triclopyr. EPA in 1998 has also made the same conclusion i n EPA R.E.D facts on triclopyr.

8. Bioequivalency

. T oxicology studies conducted with triclopyr have been performed using both the free acid and the triethylamine salt from of triclopyr. Bioequivalency of the two chemical forms of triclopyr has been addressed through the conduct of special studies with the triethylamine from of triclopyr. These studies, which included data on comparative disposition, plasma half

- life, tissue distribution, hydrolytic cleavage under physiological and environme ntal conditions for triclopyr triethylamine salt were found to adequately address the issue of bioequivalency. In addition, subchronic toxicity studies supported the pharmacokinetics data in demonstrating bioequivalence. Therefore, studies conducted with any one f orm of triclopyr can be used to support the toxicology database as a whole. On March 22, 2012 EPA (DP Barcode: D399410) made the determination that triclopyr choline and triclopyr acid are bioequivalent, thus concluding that the existing toxicol ogical database is appropriate to support the triclopyr choline evaluation.

9 . Endocrine disruption. The examination of the existing triclopyr data

- set including reproductive toxicity studies did not reveal any potential for specific
modulation of endoc rine systems in the test species. There is no evidence to suggest that triclopyr has an effect on the endocrine system.

10 . Immunotoxicity. The existing data

- set on the triclopyr does not suggest any
indication of immunotoxic potential of triclopyr. However, recently, a 28

- day immunotoxicity study was conducted on the male F344/DuCrl (most sensitive species and sex for triclopyr toxicity). Triclopyr up to 250 mg/kg/day did not caused the immunotoxicity in rats confirms the non

- immunotoxic potential of triclopyr.

1 1 . Neurotoxicity. There is no indication that triclopyr is a neurotoxic chemical and there is no need for a developmental neurotoxicity study or additional UFs to account7

for neurotoxicity, as also specified in the Triclopyr Pesticide Tolerance document (2002) (1). As part of the separate ongoing tolerance action with triclopyr in Milk and Milk Fat to support adding dairies as a use site to triclopyr technical and end use labels (OPP
Decision Number: D

- 488479 and D

- 488485) a 90

- Day dietary neurotoxicity (MRID# 49306303) study in rats was submitted. The results from that study determined a no

observed

- effect level (NOEL) for general toxicity was 25 mg/kg/day based on the decrease in body weights and feed consumption, and increased urination of the high dose males and females. There were no effects on any parameter that would suggest a neurotoxic effect, and the subchronic dietary NOEL for triclopyr technical neurotoxicity in male and female F344/DuCrl rats was 200 mg/ kg/day, the highest dose level tested. In addition to the 90

- Day dietary neurotoxicity study a weight of evidence waiver request was submitted for the acute neurotoxicity study (MRID# 49306302).

12

. Carcinogenicity

. A cancer risk assessment is not requi red. The Agency’s Carcinogenicity Peer Review Committee, according to 1986 Guideline for carcinogenic risk assessment, has established that triclopyr is classified as “Group D chemical”

– not classifiable as to human carcinogenicity (16). The guidelines on Agency’s cancer classification have been changed. According to the current Guidelines (2005) triclopyr would be classified as ‘Not likely to be carcinogenic to humans’ which would be equivalent to ‘Group D chemical’ classification per 1986 Guidelines.

C. Aggregate Exposure

1. Dietary exposure. The exposure and risk resulting from agricultural uses of triclopyr was considered for the U.S. population and special sub

- populations. There are

two direct sources of exposure to humans considering triclopyr ’s uses across all labels:
from food intake and from consuming drinking water

. The exposure and risk are estimated in this report for different durations of both routes of exposure and their aggregated contribution. In an aggregate assessment, exposures fro m food residues were combined with conservative estimates of potential water residues , as well as potential residential exposure . The current approach of the EPA Office of Pesticide Programs (OPP) is to use a tiered approach for acute dietary risk assessm ent that proceeds from very conservative assumptions about food residues, to inclusion of more realistic residue values measured closer to the point of consumption.

i. Food. The process of dietary risk assessment of pesticides considers chronic
and acut e exposures to the U.S. population and sensitive population sub

- groups. A dditional exposures from potential residues in drinking water were also combined with acute and chronic food exposure estimat ions

.

The Dietary Exposure Evaluation Model (DEEM

- FCID, version 2. 1 4), a commercially available software package, was used to estimate exposure to triclopyr via food consumption by the general U.S. population and certain subgroups. The model combined the consumption data and residue data for a given pesticide to analyze dietary
risk.8

Food consumption data from the USDA Continuing Survey of Food Intakes by Individuals (CSFII) conducted from 1994 through 1998 including the children' s supplemental survey were used in this assessment. The food consumption data, i.e., foods as consumed, were translated into raw agricultural commodities and their food forms using recipe translation files contained within the DEEM software.

a. Acute di etary exposure. EPA has established an acute reference dose (aRfD) for the purpose of the acute dietary assessment set at 0. 05 mg/kg/day for f emales 13

- 50 years old , the population sub

- group of concern. This was based on the NOAEL of 5 mg/kg/day
is based on a 2

- generation reproductive toxicity study with triclopyr acid in rats with a NOAEL of 5.0 mg/kg/day and uncertainty factor of 100. The 100

- fold safety factor includes intraspecies and interspecies variations. Exposures from all existing and proposed residues result in very low acute exposures

. Using the above assumptions for
the assessment, the food + refined water exposure to triclopyr for females 13

- 50 years old at the 95th percentile was estimated to be 0.0 0 2067 mg/kg/day that utilized 4.1 % of the
aRfD.

b. Chronic dietary exposure. EPA has established a chronic reference dose (cRfD) for triclopyr at 0.0 5 mg/kg/day for all population subgroups. The cRfD is based on a 2

- generation reproductive toxicity study in rats with a NOAEL of 5.0 mg /kg/day and uncertainty factor of 100. The 100

- fold safety factor includes intraspecies and interspecies variations. No additional FQPA safety factor is required. The food + refined

water exposure for the overall U.S. population was estimated for the as sessment to be
0.00 0 971 mg/kg/day that utilize d 1.9 % of the cRfD using the refined Tier 2 conservative exposure assumptions of 100% crop treated , tolerance values and USDA

- PDP refined
water values

. The population subgroup with the highest potential for exposure was
Children 1

- 2 years old with food + water exposure of 0.0 02 800 mg/kg/day that represented 5.6 % of the cRfD.

c. Cancer dietary exposure. A cancer risk assessment is not required

.

ii . Drinking Water

. Direct measurements of triclopyr in drinking water were
available from USDA

- PDP sources which were more realistic than e stimates of potential water concentrations resulting from agricultural use of triclopyr were using two environmental models, SCI

- GROW and GENEEC which assum es certain environmental degradation properties for triclopyr and modeled dynamics of ground water and surface
water bodies. Based on the USDA

- PDP monitoring data for the 2002

- 2003 timeframe,
the avera ge concentration from drinking water sources in multiple states across 8 99 water samples with triclopyr at or above the LOD, was 24.9 ppt (0.0000249 ppm). This number is appropriate for refined chronic dietary assessment. Based upon PDP data, water sample s were measured from 2002

- 2010, inclusive of both maximum and average concentrations from drinking water sources in multiple states. A total of 3261 water samples were analyzed for triclopyr. Of the 3261 samples, 565 had detects of triclopyr at
or above the Level of Detection (LOD). The maximum concentration during this period of time was 566 ppt (0.000566 ppm). This refined number is appropriate for refined acute dietary assessment.9

The potential, acute, aggregate exposures from food and drinking wa ter for
females 13

- 50 years old is approximately 0.0 0 2067 mg/kg

- bw/day or 4

. 3 % of the acute reference dose (aRfD) for the upper 9 5 th %tile of the population using a n assessment refined for water

.

Potential chronic exposure to water residues was estimate d using 0.0249 ppb for the two commodities, i.e., “water, direct, all sources” and “water, indirect, all sources” for input to DEEM

- FCID for chronic water (Tier II) analysis. After considering all existing and proposed uses, the exposure to triclopyr resi dues is 5.6 % of the chronic reference dose for the most exposed population sub

- group, Children 1

- 2 year s old

.

2. Non

- dietary exposure. Triclopyr is currently registered for use that could result
in short

- term and intermediate

- term residential exposure and the Agency has determined that it is appropriate to aggregate chronic food and water and short

- term exposures for triclopyr, as well as aggregate chronic food and water and intermediate

- term exposures for triclopyr

.

D. Cumulative Effects

. Dow AgroSciences has submitted to EPA an assessment of common mechanism of toxicity of triclopyr and other related compounds. Data indicate
that cumu lative toxicological effects of triclopyr with other environmental compounds are unlikely. Triclopyr also shares a common metabolite, 2,5,6

- trichloro

- 2

- pyridinol (TCP) with the insecticide chlorpyrifos / chlorpyrifos

- methyl

. The Agency found no risk
of c oncern based on the assessment of likely combined exposures to TCP from both triclopyr and chlorpyrifos / chlorpyrifos

- methyl

.

E. Safety Determination

1. U.S. population. The proposed tolerance action only adds triclopyr choline salt to the tolerance expression and does not change the existing tolerances of triclopyr as listed in 40CFR §180.417 . Therefore, there is no anticipated change in dietary exposure to triclopyr and the current chronic dietary exposure assessment that indicate s no evidence of significant toxicity and a reasonable certainty that no harm will result from exposure to residues of triclopyr is valid

.

2. Infants and children. Since there is no proposed change in the existing
tolera nces of triclopyr as listed in 40CFR §180.417 this action does not al ter EPA’s previous decision (Federal Register Vol.67, No. 181. Environmental Protection Agency. 40 CFR Part 180 [OPP

- 2002

- 0190; FR L

- 7196

- 7]. September 18, 2002):

“ There is a complete toxicity data base for triclopyr and exposure data are complete or are estimated based on data that reasonably accounts for potential exposures. The Agency has determined that the Special FQPA SF of 10x can be reduced to 1x because:

The toxicology data base is complete for FQPA special SF determination; There is no susceptibility identified following in utero exposure in rabbits;10

There is qualitative susceptibility identified following in utero as well as prenatal and postnatal exposure of the rat, however, these effects occurred at a dose (25 mg/kg/day) above the dose (5 mg/kg/day) that is used for acute and chronic dietary and residential exposure risk assessments; The developmental neurotoxicity study is not required for this chemical;
There are n o residual uncertainties associated with the exposure assessments performed for the dietary food and drinking water or the residential pathway.

In addition, the Agency determined that no traditional additional safety factor (addressing data deficiencies) is needed because:

The Agency concluded that the toxicological data base for triclopyr is complete and adequate for FQPA assessment; a developmental neurotoxicity study was not required for triclopyr and no additional safety factors are needed to account for toxicology data
deficiencies. ”

F. International Tolerances

. MRLs for residues of triclopyr have been established by EPA, Australia , Canada, and Japan

.