EPA Registration Division contact: Andrew Ertman; 703-308-9367

PP#2E8068

EPA has received a pesticide petition PP#2E8068 from BASF Corporation, Research 

Triangle Park, NC 27709 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 by establishing a 

tolerance for residues of Boscalid (BAS 510F); [3-pyridinecarboxamide, 2-chloro-N-(4'-

chloro(1,1'-biphenyl)-2-yl)-] in or on the raw agricultural commodity for Artichoke, globe at

6.0 parts per million (ppm), Berry, low growing, subgroup 13-07G at 4.5 ppm, Bushberry, 

subgroup 13-07B at 13 ppm, Caneberry, subgroup 13-07A at 6.0 ppm, Endive, Belgium at 

5.0 ppm, Fruit, citrus, group 10-10 at 1.6 ppm, Fruit, pome, group 11-10 at 3.0 ppm, Fruit,

small, vine climbing, except fuzzy kiwifruit, subgroup 13-07F, at 3.5 ppm, Oilseed, group 20

at 3.5 ppm, Persimmon at 7.0 ppm, Turnip, greens at 18.0 ppm, Vegetable, bulb group 3-07

at 3.0 ppm, Vegetable, fruiting, group 8-10 at 1.2 ppm, Vegetable, root subgroup 1B, except 

sugarbeet, at 1.0 ppm and to amend 40 CFR part 180 by removing a tolerance for residues of

Boscalid (BAS 510F); [3-pyridinecarboxamide, 2-chloro-N-(4'-chloro(1,1'-biphenyl)-2-yl)-]

in or on the raw agricultural commodity for Bushberry, subgroup 13B at 13 ppm, Caneberry, 

subgroup 13A at 6.0 ppm, Canola, seed at 3.5 ppm, Cotton, undelinted seed at 1.0 ppm, Fruit, 

citrus, group 10 at 1.6 ppm, Fruit, pome, group 11 at 3.0 ppm, Grape at 3.5 ppm, Strawberry

at 4.5 ppm, Sunflower, seed at 0.6 ppm, Vegetable, bulb, group 3 at 3.0 ppm, Vegetable, 

fruiting, group 8 at 1.2 ppm, and Vegetable, root, subgroup 1A except sugarbeet, garden 

beet, radish, and turnip at 1.0 ppm. EPA has determined that the petition contains data or 

information regarding the elements set forth in section 408(d)(2) of the FFDCA; 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. Nature of the residue studies (OPPTS Harmonized guideline 

860.1300) were conducted in grapes, lettuce and beans as representative crops in order to 

characterize the fate of boscalid (BAS 510F) in all crop matrices. In all three crops the 

boscalid (BAS 510F) Residues of Concern (ROC) were characterized as parent boscalid

(BAS 510F). A confined rotational crop study also determined that parent was the residue 

of concern in the representative crops of radish, lettuce and wheat.

2. Analytical method. In plants, the parent residue is extracted using an aqueous 

organic solvent mixture followed by liquid/liquid partitioning and a column clean up. 

Quantitation is by gas chromatography using mass spectrometry (GC/MS). In livestock 

the residues are extracted with methanol. The extract is treated with enzymes in order to 

release the conjugated glucuronic acid metabolite. The residues are then isolated by 

liquid/liquid partition followed by column chromatography. The hydroxylated metabolite 

is acetylated followed by a column clean-up. The parent and acetylated metabolite are 

quantitated by gas chromatography with electron capture detection.

3. Magnitude of residues. Field trials were carried out in order to determine the 

magnitude of the residue of boscalid (BAS 510F) in Globe artichoke, Belgium endive, and 
persimmon. Field trials were submitted previously on sunflower, rapeseed and cottonseed 

for individual tolerances; however these crops can now be considered as representative 

crops for Crop Group 20, Oilseeds. Field trials in the representative commodities for the 

following crop groups were previously submitted for crop group tolerances: Bulb Vegetable 

3-07, Fruiting Vegetable 8-10, Citrus Fruit 10-10, Pome Fruit 11-10, Caneberry subgroup 

13-07A, Bushberry subgroup 13-07B, Small Fruit Vine Climbing subgroup 13-07F and Low 

Growing Berry subgroup 13-07G. These crop groups should be updated with the recent 

crop group changes. The number and locations of field trials are in accordance with 

OPPTS Guideline 860.1500. Field trials were carried out using the maximum label rate, 

the maximum number of applications, and the minimum pre-harvest interval for each 

crop or crop group.

B. Toxicological Profile

1. Acute toxicity. Based on available acute toxicity data, boscalid and its formulated 

products do not pose acute toxicity risks. The acute toxicity studies place technical 

Boscalid (BAS 510 F) in toxicity category IV for acute oral; category III for acute dermal 

and category IV for acute inhalation. Boscalid is category IV for both eye and skin 

irritation and it is not a dermal sensitizer. For Globe artichoke, Belgium endive, and 

persimmon, the product proposed is Pristine® fungicide (BAS 516 02/04F), a water 

dispersible granule (WG) formulation containing a 2:1 mixture of boscalid (BAS 510F) and 

pyraclostrobin (BAS 500F). Pristine® fungicide (BAS 516 02/04F) has an acute oral 

toxicity category of III, acute dermal of category III, acute inhalation of category IV, eye 

irritation of category III, skin irritation of category IV, and is not a dermal sensitizer.

For the expanded crop groups, the products proposed are Endura® fungicide (BAS 510 

02/04F) containing boscalid (BAS 510F) as the active ingredient and Pristine® fungicide

(BAS 516 02/04F). Endura® fungicide (BAS 510 02/04F) has an acute oral toxicity 

category of III, acute dermal of category III, acute inhalation of category IV, eye irritation 

of category III, skin irritation of category IV, and is not a dermal sensitizer.

2. Genotoxicty. Ames Test (1 Study; gene point mutation): Negative; In Vitro 

CHO/HGPRT Locus Mammalian Cell Mutation Assay (1 Study; point gene mutation): 

Negative; In Vitro V79 Cell Cytogenetic Assay (1 Study; Chromosome Damage): Negative; 

In Vivo Mouse Micronucleus (1 Study; Chromosome Damage): Negative; In Vitro Rat 

Hepatocyte (1 Study; DNA damage and repair): Negative. Boscalid has been tested in a 

total of 5 genetic toxicology assays consisting of in vitro and in vivo studies. It can be stated 

that Boscalid did not show any mutagenic, clastogenic or other genotoxic activity when 

tested under the conditions of the studies mentioned above. Therefore, boscalid does not 

pose a genotoxic hazard to humans.

3. Reproductive and developmental toxicity. The potential reproductive and 

developmental toxicity of boscalid was investigated in a two-generation rat reproduction 

study as well as in rat and rabbit teratology studies. There were no adverse effects on 

reproduction in the two-generation study at any dose tested. The reproductive NOAEL is 

10,000 ppm (1165 and 1181 for males and females, respectively), the highest dose tested. . 

Toxicity to the offspring was seen at 1,000 ppm in the form of decreased pup weights in the 

F2 males, and at 10,000 ppm in the form of decreased pup weights for both males and 
females of both the F1 and F2 generations. The offspring NOAEL is 100 and 1000 ppm (11

and 116 mg/kg b.w./day) for males and females, respectively. In males of the F1 generation, 

reduced body weight and reduced body weight gain were observed at 10,000 ppm. 

Additionally, hepatocyte degeneration was observed in male animals of both the F0 and F1 

generations at 10,000 ppm. The parental systemic NOAEL is 1000 and 10,000 (113 and 

1181 mg/kg b.w./day) for males and females, respectively 

No teratogenic effects were noted in either the rat or rabbit developmental studies. 

In the rat study, evidence of maternal or developmental toxicity was not observed at any 

dose (highest dose tested of 1,000 mg/kg b.w./day). In the rabbit teratology study, at the 

high dose of 1,000 mg/kg b.w./day a maternal body weight gain decrease compared to 

controls of 81% was observed during the treatment period. Reduced food consumption, 

reduced body weight and abortions in three dams, were also seen at 1,000 mg/kg b.w./day. 

The NOAEL for both maternal and developmental toxicity was determined to be 300 

mg/kg b.w/day. 

Neurotoxicity was not observed at any dose in the developmental neurotoxicity 

study. Reduced pup body weights were observed at the high and mid dose levels of 1000 

and 10,000 ppm (118 and 1,183 mg/kg b.w./day, respectively). No developmental toxicity 

was seen at the low dose of 14 mg/kg b.w./day (100 ppm). Although no maternal toxicity 

was seen in this study, other studies which evaluated more parameters at similar doses of 

boscalid demonstrated maternal toxicity.

The Agency concluded that there are no residual uncertainties for pre- and 

postnatal toxicity as the degree of concern is low for the susceptibility seen in the above 

studies, and the dose and endpoints selected for the overall risk assessments will address 

the concerns for the body weight effects seen in the offspring. Although the dose selected 

for overall risk assessments (21.8 mg/kg b.w./day) is higher than the NOAEL's in the 2-

generation reproduction study (11 mg/kg b.w./day) and the developmental neurotoxicity 

study (14 mg/kg b.w./day), these differences are considered to be an artifact of the dose 

selection process in these studies. For example, there is a 10-fold difference between the 

LOAEL (113 mg/kg b.w./day) and the NOAEL (11 mg/kg b.w./day) in the two generation 

reproduction study. A similar pattern was seen with regard to the developmental 

neurotoxicity study, where there is also a 10-fold difference between the LOAEL (147 

mg/kg b.w./day) and the NOAEL (14 mg/kg b.w./day). There is only a 2-3-fold difference 

between the LOAEL (57 mg/kg b.w./day) and the NOAEL (21.8 mg/kg b.w./day) in the 

critical chronic dog study which was used for risk assessment. Because the gap between the 

NOAEL and LOAEL in the 2-generation reproduction and developmental neurotoxicity 

studies was large and the effects at the LOAEL's were minimal, the true no-observedadverse-effect-level was probably considerably higher. Therefore, the selection of the 

NOAEL of 21.8 mg/kg b.w./day from the 1-year dog study is conservative and appropriate 

for the overall risk assessments. In addition, the endpoints for risk assessment are based 

on thyroid effects seen in multiple species (mice, rats and dogs) and after various exposure 

durations (subchronic and chronic exposures) which were not observed at the LOAEL's in 

either the 2-generation reproduction or the developmental neurotoxicity studies. Based on 

these data, the Agency concluded that there are no residual uncertainties for pre- and postnatal toxicity.
4. Subchronic toxicity. The subchronic toxicity of boscalid was investigated in 90–day

feeding studies with rats, mice and dogs, and in a 28–day dermal administration study in 

rats. Additionally a 90–day neurotoxicity study in rats was performed. Generally, mild

toxicity was observed including alterations in various clinical chemistry parameters and 

effects on the liver and thyroid. In the rat, effects observed were increased thyroid weight 

and increased incidence of thyroid hyperplasia as well as follicular epithelial hypertrophy. 

Increased liver weights and an increased incidence of marked fatty changes in the liver 

were observed in mice Changes observed in dogs were increased serum alkaline 

phosphatase and liver weights. The lowest subchronic toxicity NOAEL was from the dog 

study (7.6/8.1 mg/kg b.w./day in males and females, respectively).

In the 28–day repeat dose dermal study, no systemic effects were noted up to the 

highest dose tested of 1,000 mg/kg b.w./day.

In a 90–day rat neurotoxicity study, no signs of neurotoxicity were observed in the 

pups or adults. The NOAEL is the highest tested of 15,000 ppm (1,050/1,272 mg/kg 

b.w./day in males and females, respectively).

5. Chronic toxicity. The chronic toxicity/oncogenicity studies with boscalid include a 

12–month feeding study with Beagle dogs, an 18–month B63CF1 mouse feeding study, a 

24–month Wistar rat chronic feeding study and a 24–month Wistar rat oncogenicity study. 

At the highest dose tested in dogs, effects observed consisted primarily of increased liver 

and thyroid weights and some serum clinical chemistry changes. The NOAEL was 800 

ppm (21.8 mg/kg b.w./day males; 22.1 mg/kg b.w./day females).

In the mouse oncogenicity study, decreased body weights were seen in both males 

and females at 8000 ppm (1345 and 1804 mg/kg b.w./day for males and females, 

respectively) and in males at 2000 ppm (331 mg/kg b.w./day). Also in males at 8000 ppm, 

increased liver weights and an increased incidence of peripherial hypertrophy of the liver 

were observed. The NOAEL was 400 ppm and 2000 ppm (65 and 443 mg/kg b.w./day) for 

male and female mice, respectively. 

In both the rat chronic and oncogenicity studies, the highest dose tested of 15,000 

ppm exceeded a maximum tolerated dose (MTD) and was discontinued after 17 months. 

Effects observed at the next highest dose of 2,500 ppm (110/ 150 mg/kg b.w./day for males 

and females, respectively) were increased thyroid weights and histopatholigical changes in 

the thyroid which included follicular cell hypertrophy, hyperplasia and adenomas. The 

NOAEL was 500 ppm (22 and 30 mg/kg b.w./day for male and female rats, respectively).

No evidence of treatment-induced oncogenicity was observed in the mouse study. In 

the rat, a slight increase in thyroid follicular cell adenomas was seen in both sexes at the 

high dose when the data from both chronic and oncogenicity bioassays are combined.

A non-genotoxic (threshold) mode of action (MOA) for the thyroid follicular cell 

adenomas was demonstrated from results of several studies.

Based on review of the available data, the Reference Dose (RfD) for boscalid was 

based on a 1-year feeding study in dogs with a NOAEL of 21.8 mg/kg b.w./day. Using an 

uncertainty factor of 100, the RfD is calculated to be 0.218 mg/kg b.w./day. Based on the 

acute toxicity data, an acute dietary risk assessment is not needed.

Threshold effects. 
Boscalid was shown to be non-carcinogenic in mice. There was a slight increase in 

thyroid follicular cell adenomas at the high dose in both sexes in the rat. A non-genotoxic 

(threshold) MOA was demonstrated for the thyroid tumors. The Agency concluded a 

carcinogenicity classification of “suggestive evidence of carcinogenicity” and that a dose 

response assessment for cancer was not needed.

6. Animal metabolism. In the rat, the predominant route of excretion of boscalid 

(BAS 510F) is fecal with urinary excretion being minor. The half-life of boscalid is less 

than 24 hours. Saturation of absorption appears to be occurring at the high dose level. 

Boscalid is rapidly and intensively metabolized to a large number of biotransformation 

products. The hydroxylation of the diphenyl moiety was the quantitatively most important 

pathway. Second most important was the substitution of the Cl of the 2-chloropyridine 

part against SH by conjugation with glutathione. No major differences were observed. In 

hens and goats the residues of concern were determined to be parent, the hydroxylated 

metabolite M510 F01 (2-chloro-N-(4'chloro-5-hydroxy-biphenyl-2-yl)nicotinamide), and 

the glucuronic acid of the metabolite M510 F02.

7. Metabolite toxicology. No additional studies were required for metabolite 

toxicology.

8. Endocrine disruption. No specific tests have been conducted with boscalid to 

determine whether the chemical may have an effect in humans that is similar to an effect 

produced by a naturally occurring estrogen or other endocrine effects. However, there 

were no significant findings in other relevant toxicity studies (i.e., subchronic and chronic 

toxicity, teratology and multi-generation reproductive studies) which would suggest that 

boscalid produces endocrine related effects.

C. Aggregate Exposure

1. Dietary exposure. An assessment was conducted to evaluate the potential risk due 

to chronic dietary exposure of the U.S. population and sub-populations to residues of 

boscalid. Tolerance values for boscalid (BOSCALID) have previously been established and 

are listed in U.S. 40 CFR § 180.589. This analysis included all crops with established 

boscalid tolerance values, new tolerances for artichoke, Belgium endive and persimmon 

and tolerances for the updated crop groups 3-07, 8-10, 10-10, 11-10, 13-07A, 13-07B, 13-

07F, 13-07G and 20.

i. Food. 

Acute Dietary Exposure Assessment

An acute assessment was not needed since the U.S. EPA Toxicological Endpoint Selection 

(TES) Committees had previously evaluated the boscalid toxicity data and determined 

there were no toxic effects attributable to a single dose. Therefore, a quantitative acute 

dietary exposure and risk assessment were not required.

Chronic Dietary Exposure Assessment

A partially refined Tier 1 chronic dietary exposure assessment was conducted assuming 

tolerance level residues, experimentally determined processing factors, 100% crop treated 

factors for all crops and NHANES Consumption data from 2003-1008 using version 3.14 of 

the Dietary Exposure Evaluation Module (DEEM-FCID) software. Residues in animal 
commodities (i.e. meat, meat byproducts, fat, milk, eggs) were included at the tolerance 

levels currently established and listed in U.S. 40 CFR § 180.589. 

Dietary exposure estimates were compared against the established boscalid chronic 

Population Adjusted Dose (cPAD) of 0.218 mg/kg b.w./day for all populations. Results of 

the chronic dietary assessments are listed in the Table 1. The estimated chronic dietary 

exposure from crops and animal commodities was less than 28% of the cPAD for all 

subpopulations. Additional refinements such as the use of anticipated residues and 

adjusted crop treated factors would further reduce the estimated chronic dietary exposure. 

The results in Table 1 demonstrate there are no safety concerns for any subpopulation 

based on established and new uses, and the results clearly meet the FQPA standard of 

reasonable certainty of no harm.

Table 1. Summary of Chronic Dietary Exposure Assessment 

Considering Crops with Established and Proposed Tolerances

for Boscalid

Population

Subgroups

Exposure Estimate

(mg/kg b.w./day) %cPAD

U.S. Population 0.020542 9.4

All Infants 0.035194 16.1

Children 1-2 years 0.059105 27.1

Children 3-5 years 0.043517 20.0

Children 6-12 years 0.02428 11.1

Youth 13-19 years 0.013975 6.4

Adults 20-49 years 0.017067 7.8

Adults 50+ years 0.018957 8.7

Females 13 - 49 0.01734 8.0

%cPAD = percent of chronic population adjusted dose 

Exposure estimates based on tolerance values, default processing 

factors, and 100% CT for all crops/commodities.

ii. Drinking water. 

Based on PRZM/EXAMS and SCI-GROW models, the estimated drinking water exposure 

concentrations of boscalid for chronic exposure were 26 ppb for surface water and 0.63 

ppb for ground water. Drinking water contributions were assessed based on the maximum 

estimated boscalid water concentrations (26 ug/L), and water consumption and body 

weights reported in NHANES 2003-1008 Consumption surveys, using version 3.14 of the 

DEEM-FCID software. The chronic estimated water exposure values are summarized in 

Table 2. Minimal exposure of boscalid occurs through drinking water with < 1.0% cPAD 

for all subpopulations.
Table 2. Results for Boscalid Chronic Water Exposure Analysis Considering the 

Maximum Estimated Chronic Drinking Water Concentration using 

DEEM-FCID 

Population Water Exposure Estimate %aPAD

Subgroups (mg/kg b.w./day)

U.S. Population 0.000544 0.2

All Infants (< 1 year old) 0.001404 0.6

Children (1-2 years old) 0.000785 0.4

Children (3-5 years old) 0.000662 0.3

Children (6-12 years old) 0.000477 0.2

Youth (13-19 years old) 0.000397 0.2

Females (13-49 years old) 0.000543 0.2

Adults (20-49 years old) 0.000537 0.2

Adults (50+ years old) 0.000541 0.2

cPAD = chronic population adjusted dose

Based on estimated acute surface water value of 26 ug/L

Acute Aggregate Exposure and Risk (Food and water)

Since the U.S. EPA Toxicological Endpoint Selection (TES) Committees has evaluated the 

Boscalid toxicity data and determined there was no toxicological endpoints for acute 

dietary exposure, the determination of an acute aggregate exposure and risk evaluation 

was not required. 

Short- and Intermediate Term Aggregate Exposure and Risk (food,water, and residential)

Short- and intermediate-term aggregate exposure takes into account residential exposure 

plus chronic exposure from food and water. Residential exposure is used to refer to nonoccupational and non-dietary exposure. No new residential uses are currently being 

registered for boscalid that would increase non-dietary exposure. The residential exposure 

value used in this risk assessment was previously determined by the EPA (Federal Register, 

Volume 68, No 146, July 30, 2003) and considers dermal exposure to adults from the golf 

course use. The MOE presented in the Table 3 is considered to be representative for youth 

playing golf because youth and adults possess similar body surface area to weight rations 

and because the dietary exposure for youth (13-19 years old) is less than that of the general 

US population. 

Table 3. Estimated Short/Intermediate Term Aggregate Exposure and Risk of 

Boscalid 
Population

NOAEL 

(mg/kg/day)

Target 

MOE1

Food 

Exposure 

(mg/kg/day)

Water 

Exposure 

(mg/kg/day)

Residential 

Exposure2

(mg/kg/day)

Total 

Exposure 

(mg/kg/day) MOE3

US 21.8 100 0.020542 0.000544 0.0008 0.021886 996 1 Target MOE is 100.

2

 Residential Exposure = Exposure to adult while playing golf.

3 Aggregate MOE = (NOAEL / (Food + Water + Residential Exposure)

Chronic Aggregate Exposure and Risk (food and water) 

The aggregate chronic risk includes residues of boscalid from food and water (Table 4). 

Exposures from residential uses are not included in the chronic aggregate assessment. The 

results demonstrate there are no safety concerns for any subpopulation based on 

established and new uses, and that the results clearly meet the FQPA standard of 

reasonable certainty of no harm. 

 Table 4. Estimated Chronic Aggregate Exposure and Risk of Boscalid

Population Subgroup

cPAD 

(mg/kg/day)

Food 

Exposure 

(mg/kg/day)

Water 

Exposure 

(mg/kg/day)

Total 

Exposure 

(mg/kg/day)

%

cPAD

U.S. Population 0.218 0.020542 0.000544 0.021086 10

All Infants (< 1 yr old) 0.218 0.035194 0.001404 0.036598 17

Children 1-2 years 0.218 0.059105 0.000785 0.05989 27

Children 3-5 years 0.218 0.043517 0.000662 0.044179 20

Children 6 – 12 years 0.218 0.02428 0.000477 0.024757 11

Youth 13-19 years 0.218 0.013975 0.000397 0.014372 7

Adults 20-49 years 0.218 0.017067 0.000543 0.01761 8

Adults + 50 0.218 0.018957 0.000537 0.019494 9

Females 13 - 49 0.218 0.01734 0.000541 0.017881 8

2. Non-dietary exposure. No new residential uses are currently being registered for 

boscalid that would increase non-dietary exposure. A non-occupational dermal postapplication exposure/risk assessment for individuals golfing and harvesting fruit at “UPick” farms and orchards was previously conducted by EPA (Federal Register, Volume 68, 

No 146, July 30, 2003). Because U-Pick is a one-time event (duration < 1 day) and the EPA 

found that the oral studies indicated there were no endpoints appropriate to quantitate 

acute risk. Therefore, only the golfing scenario was evaluated with respect to nonoccupational, non-dietary exposure. The dermal MOE’s for adults playing golf were 

27,000 – 74,000. Although specific MOE’s were not calculated for youths playing golf, the 

adult MOEs are considered representative since the body surface area to weight ratios for 

adolescents do not vary significantly from those of adults.
D. Cumulative Effects

Section 408(b)(2)(D)(v) requires that, when considering whether to establish, 

modify, or revoke a tolerance, the Agency consider ‘‘available information’’ concerning the 

cumulative effects of a particular pesticide’s residues and ‘‘other substances that have a 

common mechanism of toxicity.’’ BAS 510 F is a foliar fungicide chemically belonging to 

the carboxin class of fungicides. BAS 510 F acts in the fungal cell by inhibiting 

mitochondrial respiration through inhibition of the succinate-ubiquinone oxidase reductase 

system in Complex II of the mitochondrial electron transport chain. BAS 510 F shares this 

mode of action with only one other currently registered U.S. pesticide - carboxin. 

The EPA is currently developing methodology to perform cumulative risk 

assessments. At this time, there is no available data to determine whether BAS 510F has a 

common mechanism of toxicity with other substances or how to include this pesticide in a 

cumulative risk assessment. Unlike other pesticides for which EPA has followed a 

cumulative risk approach based on a common mechanism of toxicity, BAS 510F does not 

appear to produce a toxic metabolite produced by other substances.

E. Safety Determination

1. U.S. population. Based on this risk assessment, BASF concludes that there is a 

reasonable certainty that no harm will result to the general population from the aggregate 

exposure to boscalid residues.

2. Infants and children. Based on this risk assessment, BASF concludes that there is a 

reasonable certainty that no harm will result to infants or children from the aggregate 

exposure to boscalid residues.

F. International Tolerances

Several maximum residue levels (MRL) have been established for Boscalid (BAS 

510F) in multiple plant and animal commodities by the Codex Alimentarius Commission.

National and Import MRLs have also been established for multiple commodities in several 

countries in all regions of the world.