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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

4F8249

EPA has received a pesticide petition 4F8249 from Dow AgroSciences LLC, 

9330 Zionsville Road, Indianapolis, IN 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 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 0.03 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 

have 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. 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 
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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. Three 

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

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

each cow was sampled by combining 1⁄2 pint from the evening milking with an equal 

amount collected following morning. Cream samples were collected from the morning 

milk by pooling 11⁄2 gallon of milk from each cow at 100 or 1000 ppm doses. The revised 

tolerance of triclopyr in milk is 0.03 ppm and the new tolerance in milk fat is 0.70 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. 

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.
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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 

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 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.

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 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 water consumption, and increased relative kidney and liver 
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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 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 
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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 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. 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 
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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-trichloro2-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 bioequivalency. In addition, 

subchronic toxicity studies supported the pharmacokinetics data in demonstrating 

bioequivalence. Therefore, studies conducted with any one form of triclopyr can be used 

to support the toxicology database as a whole.

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

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).

12. 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.
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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 2.14), 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 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 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

at the 95th percentile was estimated to be 0.002067 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 0.05 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 
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water exposure for the overall U.S. population was estimated for the assessment to be 

0.000971 mg/kg/day that utilized 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 0.002800 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 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). This number 

is appropriate for refined chronic dietary assessment. 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 

acute dietary assessment. 

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

years old is approximately 0.002067 mg/kg-bw/day or 4.3 % 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 0.0249 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 residues is 5.6 % 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 

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. 
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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, and milk fat using tolerance values and 

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

of 1.9% of cRfD for the general U. S. population when the amended 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 4.1 % 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 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 1.8 % of the cRfD for All Infants (<1 yr old), 5.6 % of the cRfD for 
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children 1-2 yrs old and 4.3 % 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

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.