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EPA REGISTRATION DIVISION COMPANY NOTICE OF FILING FOR PESTICIDE 

PETITIONS PUBLISHED IN THE FEDERAL REGISTER 

EPA Registration Division contact: Reuben Baris (703)305-7356 

Dow AgroSciences LLC

4F8249 

EPA has received a pesticide petition (4F8249) 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. 346a(d), to amend 40 

CFR part 180.417(a)(1) by establishing a tolerance for residues of triclopyr, [(3,5,6-

trichloro-2-pyridinyl)oxy]acetic acid, including its metabolites and degradates, in or on 

the raw agricultural commodity milk, fat at 0.7 ppm, and increasing the tolerance in milk

from 0.01 ppm to 0.6 ppm; and to amend 40 CFR part 180.417(a)(2) by establishing

tolerances for the combined residues of triclopyr, [(3,5,6-trichloro-2-pyridinyl)oxy]acetic 

acid and its metabolite 3,5,6-trichloro-2-pyridinol (TCP), calculated as the stoichiometric

equivalent of triclopyr in or on the raw agricultural commodities cattle, goat, hog, horse, 

and sheep meat byproducts at 0.7 ppm; by increasing tolerances in cattle, goat, hog, 

horse, and sheep fat from 0.05 ppm to 0.09 ppm; and by increasing tolerances in cattle, 

goat, hog, horse, and sheep meat from 0.05 ppm to 0.08 ppm. EPA has determined that 

the petition contains data or information regarding the elements 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 milk fat 

(cream). EPA has established that the qualitative nature of the residue is adequately 

understood based on two studies with [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-tricihloro-2-pyridinol and 2-methoxy-3,5,6-

trichloropyridine were detected. The 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 methods 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 (MRIDs 
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00070045 and 41961001). 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 located 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. Grass 

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 triclopyr 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.

An acceptable dairy cattle feeding study has been submitted to the Agency. Four lactating 

Friesian/Holstein dairy cows were fed with diets containing triclopyr in increasing doses 

for four-week period per dose at rates equivalent to 0-1000 ppm feed. Daily whole milk 

from each cow was collected. For each cow a combined proportional sample was 

constructed from the PM and AM samples, on the basis of milk yields recorded at the 

corresponding milkings sampled. Cream samples were collected from the combining 

evening morning milk by pooling 2 quarts of milk from each cow at each dose on Days 

22 and 26. Tissue samples were collected from each cow immediately after slaughter.

The revised tolerance of triclopyr in milk is 0.6 ppm and the new tolerance in milk fat is 

0.70 ppm. The revised tolerance of triclopyr and its metabolite TCP (calculated as the 

stoichiometric equivalent of triclopyr) in meat is 0.08 ppm, in fat is 0.09 ppm and 

deletion of kidney and liver tolerance and establishment of meat, byproducts (including 

liver and kidney) at 0.08 ppm. These proposed tolerances were derived from the worst 

case animal dietary burden, which was estimated from grass commodities containing 

triclopyr at tolerance levels of 700 ppm for grass forage and 200 ppm for grass hay and 

are adequate to allow grazing of lactating dairy cattle on pasture or rangeland treated with 

triclopyr formulations according to label.

B. Toxicological Profile

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

triclopyr-TEA and triclopyr-BEE. 
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i. For triclopyr acid, the acute oral LD50 was 729 mg/kg for males and 630 mg/kg for 

females; 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 skin but was a skin sensitizer.

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 sensitizer.

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 next 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 reference 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 increased 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 exposure 

assessment are females (13-50 years old).

2. Genotoxicty.

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 hostmediated 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 primary 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 hepatic 

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 

concluded that, triclopyr is not mutagenic or genotoxic.

3. Reproductive and developmental toxicity.
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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 clinical signs. 

The developmental NOAEL was 100 mg/kg/day and developmental LOAEL was 200 

mg/kg/day based on increase 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 

water 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.

iii. 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 mortality. 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.

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 based 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 embryonic deaths due to 

abortions.

vi. 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 proximal 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. Subchronic 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 
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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 packed 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).

iii. 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.

iv. 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 and not of toxicological significance.

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 dog 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 
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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.

Carcinogenicity. A cancer risk assessment is not required. 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.

6. Animal metabolism. Disposition and metabolism 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 radioactivity, 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 significant 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 in EPA R.E.D facts on triclopyr.

8. Bioequivalency. Toxicology 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 environmental conditions for triclopyr triethylamine 

salt were found to adequately address the issue of bioequivalence. In addition, subchronic 

toxicity studies supported the pharmacokinetics data in demonstrating bioequivalence.

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

including reproductive toxicity studies did not reveal any potential for specific 

modulation of endocrine 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 
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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.

11. 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 account 

for neurotoxicity, as also specified in the Triclopyr Pesticide Tolerance document (2002).

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 from 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 assessment 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 acute exposures to the U.S. population and sensitive population sub-groups.

Additional exposures from potential residues in drinking water were also combined with 

acute and chronic food exposure estimations.

The Dietary Exposure Evaluation Model (DEEM-FCID, version 4.02), 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. 

Food consumption data from NHANES/WWEIA food consumption survey data, i.e., the 

2005-2010 data 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 dietary 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 females 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
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at the 95th percentile was estimated to be 0.025328 mg/kg/day that utilized 51% of the 

aRfD.

b. Chronic dietary exposure. EPA has established a chronic reference dose (cRfD) for 

triclopyr at 0.05 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 assessment to be 

0.004447 mg/kg/day that utilized 8.9% 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 0.026612 mg/kg/day that 

represented 53% 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 estimates of potential 

water concentrations resulting from agricultural use of triclopyr were using two

environmental models, SCI-GROW and GENEEC which assumes 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 average concentration from drinking water sources in multiple states across 899 water 

samples with triclopyr at or above the LOD, was 24.9 ppt (0.0000249 ppm). Based upon 

PDP data, water samples 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 chronic dietary assessment. The appropriate maximum concentration in water for 

the acute dietary assessment is 400 ppm set from the Drinking Water Level of Concern 

(DWLOC) of 0.4 ppm (400 ppb) established as part of the registration of the aquatic uses 

of triclopyr dimethyl amine.

The potential, acute, aggregate exposures from food and drinking water for females 13-50 

years old is approximately 0.025328 mg/kg-bw/day or 51% of the acute reference dose 

(aRfD) for the upper 95th %tile of the population using an assessment refined for water.

Potential chronic exposure to water residues was estimated using 0.566 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 residues is 53% of the chronic reference dose for 

the most exposed population sub-group, Children 1-2 years old.

2. Non-dietary exposure. Triclopyr is currently registered for use that could result 
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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 cumulative 

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 concern 

based on the assessment of likely combined exposures to TCP from both triclopyr and 

chlorpyrifos / chlorpyrifos-methyl.

E. Safety Determination

1. U.S. population. Using the above conservative exposure assumptions and 

taking into account the completeness and reliability of the toxicity data, acute and chronic 

dietary food exposure to triclopyr from milk, milk fat and fat using tolerance values and 

refinement (Tier 2) of the water values using USDA-PDP data, resulted in risk estimates 

of 8.9% of cRfD for the general U. S. population when the amended fat tolerance, milk 

tolerance and additional milk fat tolerance was included in the assessment with all 

existing uses of triclopyr. Generally, EPA has no concern for exposures below 100% of 

the chronic reference dose (cRfD) because the cRfD represents the level at or below 

which daily dietary exposures over a lifetime will not pose appreciable risks to human 

health. 

Likewise, the acute dietary food exposure at 95th percentile for females 13-50 years old, 

the population sub-group of concern is 51% of acute reference dose (aRfD). Therefore, 

there is no concern for exposure because the acute RfD represents the level at or below 

which a single daily exposure will not pose appreciable risks to human health.

Cancer dietary risk assessment was not required.

Short-term and intermediate-term risks are considered appropriate to aggregate with 

chronic food and water exposures for triclopyr. Adjusting for the above newly calculated 

exposure for food and water (mg/kg per day) resulting from amended and proposed 

tolerances, short- and intermediate-term aggregate MOEs do not exceed the LOC. 

Therefore, based on these risk assessments, Dow AgroSciences concludes that there is 

reasonable certainty that no harm will result to the U. S. population from aggregate 

exposure to triclopyr residues.

2. Infants and children. EPA uses a weight evidence approach in determining 

what safety factor is appropriate for assessing risks to infants and children. This approach 

takes into account the nature and severity of the effects observed in pre- and post-natal 
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studies and other information such as epidemiological data. The completeness and 

adequacy of the toxicity database is also considered.

Toxicity database and exposure data for triclopyr are complete. EPA has considered in 

utero and/or postnatal exposure in the acceptable prenatal developmental toxicity studies 

with rat and rabbits as well as in a 2-generation reproductive toxicity study in rats. EPA 

has previously determined that no additional safety factor to protect infants and children 

is necessary for triclopyr for assessing risk to infants and children.

Using the conservative assumptions described above, the chronic dietary exposure to 

triclopyr will utilize 14% of the cRfD for All Infants (<1 yr old), 53% of the cRfD for 

children 1-2 yrs old and 29% of the cRfD for children 3-5 yrs old. In assessing the 

potential for additional sensitivity of infants and children to residues of triclopyr, data 

from developmental toxicity studies in rats and rabbits and a 2-generation reproduction 

study in the rat are considered. The developmental toxicity studies are designed to 

evaluate adverse effects on the developing organism resulting from pesticide exposure 

during prenatal development. Reproduction studies provide information relating to effects 

from exposure to the pesticide on the reproductive capability and potential systemic 

toxicity of mating animals and on various parameters associated with the well-being of 

offspring. The completeness and adequacy of the toxicity data base is also considered. 

EPA has previously determined that no additional safety factor to protect infants and 

children is necessary for triclopyr and that the RfD of 0.05 mg/kg/day is appropriate for 

assessing risk to infants and children.

Therefore, based on the completeness and reliability of the toxicity data and the 

conservative exposure assessment, Dow AgroSciences concludes with reasonable 

certainty that no harm will result to infants and children from the aggregate exposure to 

triclopyr from all current and proposed ending uses. 

F. International Tolerances

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

Japan. Based upon a review of the tolerance values it can be concluded that the tolerances 

in milk and related commodities are not harmonized. The disharmony may be attributed 

to differing definitions of the milk commodity and the corresponding fat content.