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**EPA REGISTRATION DIVISION COMPANY NOTICE OF FILING FOR PESTICIDE PETITIONS PUBLISHED IN THE FEDERAL REGISTER**  **EPA Registration**  **Division contact: Tony Kish, (703) 308** 
**- 9943** 

**INSTRUCTIONS: Pl**  **ease utilize this outline in preparing the pesticide petition. In cases where the outline element does not apply, please insert “NA** 
**- Remove” and**  **maintain the outline. Please do not change the margins, font, or format in your pesticide petition. Simply repl**  **ace the instructions that appear in green**  **, i.e., “ [**  **insert company name**  **] ,” with the information specific to your action.**  **TEMPLATE: Interregional**  **Research Project Number 4 (IR**
**- 4)**  **2F7977** EPA has received a pesticide petition **2F7977** from **ISK Biosciences Corporation, 7470 Auburn Road, Suite A,**  **Concord, Ohio 44077 ,**  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 f or residues of **f**

**luazinam** in or on the raw agricultural commodity **soybean , seed**  at **0. 0**  **1** parts per million (ppm) **and soybean, hulls at 0.02 ppm** . EPA has determined that the petition contains data or information regarding the elements set forth in section 4 08 (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 Plant metabolism. **The residue of concern is best defined as the parent, fluazinam in most crops and as the parent, fluazinam and its metabolite, AMGT, in fruit crops**  **(grape and blueberry). The metabolism of flua** **zinam in plants (potatoes, peanuts, apples and wine grapes) is adequately understood for the purposes of these**  **tolerances. The metabolism of fluazinam in peanut and potato involves initial reduction of the nitro groups, hydrolysis of the trifluoromethyl g**  **roup as well as replacement of chlorine by glutathione with subsequent reactions along the**  **glutathione pathway. Following replacement of the deactivating NO2 and Cl groups with activating groups such as OH, NH2 and sulfhydryl, ring cleavage occurs.**  **Paren t fluazinam is then rapidly degraded to form CO2 and carbon fragments**  **which are incorporated into natural products such as glucose, fructose, sucrose, oils**2

**and protein. Thus, parent fluazinam is either not found or barely detectable in peanuts and potatoe**  **s. Fluazinam parent was the major identifiable residue in both the grape and apple metabolism studies. However, minor levels of AMGT (less than**  **5% of the total radioactive residue) were also formed in grapes and apples. In grape and apple metabolism stu**  **dies, following reduction of the nitro groups and replacement of chlorine with a sulfur containing side** 
**- chain such as glutathione (as**  **occurred in peanuts and potatoes), glucose is attached to the thiolactic acid conjugate of AMPA to form the metabolite kno**  **wn as AMGT. This metabolite was not found in**  **the peanut or potatoes metabolism studies. It is analogous to the cysteine conjugate of AMPA found in rats. Identifiable residues in plant**  **metabolism studies either closely resemble flua zinam in structure or are the result**  **of re**
**- incorporation of the fluazinam carbon pool into natural products.**  **Ruminant and poultry metabolism studies demonstrated that the transmittal of residues from the feed of goats and hens through to meat, milk, a**  **nd eggs was low. Total 14C residues were below 1 ppm in all tissues, milk and eggs. Identifiable**  **residues were less than 2% of the administered dose in all matrices, except for chicken fat and liver**  **. The major metabolite found in animal tissues and milk w**  **ere DAPA, AMPA, and their sulfam**  **ate conjugates. Parent Fluazinam was only detected in very small amounts**  **.** 2. Analytical method. **An analytical method using LC** 
**- MS/MS**  **for the determination of fluazinam**  **and AMGT residues on**  **soybeans has been developed**  **a nd validated. The method involves solvent extraction followed by liquid** 
**- liquid**  **partitioning and concentration prior to a final purifica tion**  **. The method has been successfully validated by an independent laboratory using peanut nutmeat as the**  **ma trix. The**  **limit of quantitation (LOQ) of the method is 0.0 1**  **ppm for both**  **fluazinam and AMGT in**  **both crops .**  3. Magnitude of residues. **A total of 1 6**  **field trials were conducted on soybeans**  **. Treatment**  **2 of each field site consisted of two (2**  **) foliar applications a t the target**  **rate of approximately 0. 50**  **lb a.i./A, applied at**  **9**
**- 16**  **day intervals .**  **Two decline trial**  **s were**  **included with sampling at 10**  **, 20**  **and 40**  **days after the last application. Forage**  **was harvested**  **at each site at 29**
**- 35**  **day s after the last**  **application. Fluazinam**  **residues ranged from 0.072 ppm to 11.978 ppm, while AMGT was not detected in any forage sample.**  **Hay samples were cut and allowed to dry resulting in pre**
  ** harvest intervals (PHI’s) of 31**
**- 72 days.**  **Fluazinam residues ranged from 0.024 ppm to 7.26**  **4 ppm in hay and again no detectable AMGT was observed. A feeding**  **restriction will be place on the label for these items. Soybean seed samples had**  **PHI’s from 56 to 94 days excluding the decline trials. The results show that**  **no detectable residues of**  **Flu azinam**  **or AMGT at**  **the LOD (0.003 ppm) were found in**  **soybean seed, even at PHI’s as short as 36 days. Fluazinam**  **residue s**  **were below the LOQ**  **in the aspirated grain fraction. A processing study was conducted at a 10X rate that resulted in no concentration o**  **f residues in soybean meal or refined oil. Residues of Fluazinam did concentrate at a 5X level in the hulls.**  **No residues of AMGT were observed in any sample**  **, even at the 10X rate .** 3

B. Toxicological Profile 1. Acute toxicity. **A battery of acute to xicity studies was conducted which**  **placed technical fl uazinam in Toxicity Category IV for**  **acute oral LD50 and**  **dermal irritation,**  **and Category II**  **I for**  **dermal LD50, inhalation LC50 and eye irritation.**  **Technical fluazinam showed potential for dermal sensitiz ation. In an acute**  **neurotoxicity study, the NO A** **EL for neurotoxicity was 2000 mg/kg bw (the highest dose tested) and the NO**  **A EL for systemic effects was 50 mg/kg bw.**  2. Genotoxicty. **A battery of tests has been conducted to assess the genotoxic potential**  **of technical fluazinam. Assays conducted included two gene mutation tests in bacteria, a chromosomal aberration test in mammalian cells, a mouse**  **micronucleus test and a DNA repair test in bacteria. Technical fluazinam did not elicit a genotoxic response**  **in any of the studies conducted .**  3. Reproductive and developmental toxicity. **In a two -**  **generation reproductive toxicity study, the**  **NOAEL for reproductive effects was 100 ppm (10.**  **6 mg/kg**  **bw/day). The NOAEL**  **for parental toxicity was 20 ppm ( 1.9**  **mg/kg bw /day).**  **In a rat developmental study, there were no developmental effects observed at non**  **- maternally toxic doses. The developmental**  **NOAEL was 50 mg/kg bw/day and**  **the LOAEL**  **was 250 mg/kg bw/day, base d upon**  **decreased mean fetal body weight and other evi**  **dence suggestive of delayed fetal development related to maternal toxicity. The maternal**  **NOAEL was shown to be 50 mg/kg bw/day.**  **In a rabbit developmental study, there were no developmental effects observed at non**  **- maternally toxic doses. The developme**  **ntal NOAEL**  **was 7 mg/kg bw/day and the**  **LOAEL was 12 mg/kg bw/day, based on increased incidence of total litter loss**  **and possible slightly increased incidences of fetal findings at this dose. It was concluded that the m**  **aternal NOAEL**  **was 4 mg/kg bw/day .**  4

. Subchronic toxicity. **The NOAEL**  **for the 13**
**- week feeding study in rats was**  **50 ppm ( 3.8**  **mg/kg bw/day in males, 4.3**  **mg/kg bw/day in females**  **). The LOAEL**  **was 500 ppm ( 38**  **mg/kg bw/day in males, 44**  **mg /kg bw/day**  **in females ), based on**  **periacinar hepatocellular hy pertrophy and sinusoidal chronic inflammation in**  **males, increased liver weights in males and increased lung weights in females. In a 13** 
**- week dog study, the**  **NOAEL was 10 mg/kg bw/day. The**  **LOAEL was 100**  **mg/kg bw/day, based on ocular change observed opht halmoscopically and liver**  **effects consisting of increased relative liver to body weight, bile duct hyperplasia with or without cholangiofibrosis and increased plasma phosphatase levels.**  **In a 21**
**- day dermal study, the**  **NOAEL for systemic effects was 10 mg** **/kg bw/day. The**  **LOAEL was 100 mg/kg bw/day, based on hepatocelluar hypertrophy and**  **increases in AST and cholesterol levels. In a subchronic neurotoxicity study, no effects considered to be indicative of**  **neurotoxicity were observed at the highest dose tested, 3000 ppm (233 mg/kg bw/day**  **in males, 2**  **80 mg/kg bw/day**  **in females ). The**  **NOAEL for systemic toxicity (body**  **weight differences) was 1000 ppm (74 mg/kg bw/day).**4

**In a developmental neurotoxicity study in rats, fluazinam was administered by gavage**  **to female rats from Day 6 after mating to Day 20 of lactation and additionally to their offspring from Day 7 of age to Day 20 or 21 of age. The**  **author concluded that the**  **ma ternal**  **NOAEL was 2 mg/kg bw/day based on reduced body**  **weights and lower food intak e. No effects were seen on the microscopic structure of**  **the nervous system of the dams at any dose level (maximum dose of 50 mg/kg bw/day). The NOAEL for behavior and nervous system of the dams was**  **> 50 mg/kg**  **bw/day , the highest dose tested**  **. No adverse e ffect of treatment at any dose level was**  **seen on number of implantations, litter size or offspring survival. Signs of general toxicity in the offspring were evident based on lower Day 1 body weights and lower**  **weight gains at 10 and 50 mg/kg bw/day through weaning. The**  **NOAEL for general**  **toxicity to offspring was 2 mg/kg bw/day. There was no evidence of developmental neurotoxicity in the offspring. The NOAEL for the functional and morphological**  **development of the nervous system in the offspring was >**  **50 mg /kg bw/day**  **, the highest dose tested**  **. There was no increased sensitivity of the fetus or young rat pups to fl**  **uazinam as compared to the dams .**  5. Chronic toxicity. **Fluazinam was not carcinogenic in rats. A NOAEL**  **of 10 ppm (** **Males: 0.**  **38 mg/kg bw/day**  **; Fem ales:**  **0. 47**  **mg/kg bw/day ) of fluazinam was**  **established based on the following effects at 1000 and/or 100 ppm: lower food consumption and efficiency of food utilization, slight anemia, elevated cholesterol,**  **increased liver weights, an increased number of mac roscopic liver and testes lesions**  **and an increased incidence of microscopically observed lung, liver, pancreas, lymph node and testes lesions.**  **An additional study was conducted to further define the NOAEL**  **for long**
**- term**  **effects in the rat. In the secon d study, a**  **NOAEL of 50 ppm (2.2 mg/kg bw/day) was**  **established based on liver and testes effects. Two long**  **- term feeding studies were conducted in mice. In the first, the**  **NOAEL for all effects was 10 ppm (** **Males: 1.1 mg/kg bw/day**  **; Females: 1.2 mg** **/kg bw/d ay** **) and the**  **LOAEL was 100 ppm (** **Males: 10.7 mg/kg bw/day**  **; Females: 11.7 mg/kg**  **bw/day ) based on the treatment** 
**- related effects observed in the liver.**  **A second oncogenicity study in mice was conducted at 1000, 3000 and 7000 ppm to ensure that an MTD dose w**  **as studied. Findings included increased female mo**  **rtality, reduced body weight gains, increased brain weights and/or liver weights. An impurity in the test material used in this study resulted in vacuolation of the**  **white matter of the brain and cervical s pinal cord in treated animals. A statistically**  **significant higher incidence of hepatocellular adenomas was observed in the 3000 ppm dose males. Hepatocellular adenomas are common tumors in male mice.**  **There was no dose relationship in the induction of the adenoma and no increase in**  **hepatocellular carcinomas. It was**  **concluded that fluazinam is not carcinogenic in the mouse.**  **In a chronic dog study, the NOAEL**  **was determined to be 1 mg/kg bw/day. The LOAEL**  **was 10 mg/kg bw/day based on generalized, nonsp ecific toxicity. No ocular**  **effects were observed ophthalmosco pally at any dose in this study**  **.**5
6. Animal metabolism. **After an oral dose of fluazinam the median peak time for blood concentration of radiolabel activity for both sexes was 6 hours. The ma**  **jor route of excretion was the feces with urine contributing as a minor route. Less than**  **1% of the administered dose was found in the terminated animals. The highest concentration**  **in tissues was found in the liver. There were no major differences**  **related to sex or dose level in the findings. It was concluded that fluazinam is**  **metabolized by both reduction and glutathione and glucuronide conjugation and further metabolism**  **.** 7. Metabolite toxicology

. **The same metabolic processes occur in plants and anim**  **als but metabolism in plants is more extensive than in animals. All of the major identified metabolites in both plants and animals retain the phenylpyridinylamine**  **structure. Many of the metabolites resulting from fluazinam are similar in plants and animal**  **s and, therefore, have already been evaluated toxicologically. Because of the rapid and complete elimination (in animals) and re** 
**- incorporation**  **(in plants) of fluazinam, the toxicity of metabolites is expected to be similar to but lower than the toxic** **ity of the parent compound. The residue of concern is parent fluazinam only in most crops and parent fluazinam plus its minor metabolite**  **AMGT on/in fruit crops such as grape and blueberry .**  8. Endocrine disruption

. **The toxicological profile of fluazina m shows no**  **evidence of physiological effects characteristic of the disruption of the hormone estrogen in mammalian chronic studies or in mammalian or avian reproduction**  **studies. It is therefore considered that there is an adequate level of safety over th e**  **reference dose for possible endocrine effects and that an additional safety factor for possible endocrine effects is not warranted**  **.** C. Aggregate Exposure 1. Dietary exposure. **Potential dietary exposures from food were estimated using the proposed**  **tolerances for all crops (except apples as noted below),**  **using the Dietary Exposure Evaluation Model** 
**- Food Consumption Intake Database (DEEM** 
**** **FCID TM** **) and percent crop treated of 100% (with the exception of imported wine grapes as discussed below). The follo** **wing raw agricultural commodities were included: apple, carrot, brassica (cole) leafy vegetables (Group 5) including turnip**  **greens, bean (Groups 6A, 6B and 6C), bushberry (Group 13**
**- 07B), ginseng, head**  **lettuce, leaf lettuce , bulb onion (Crop 3** 
**- 07A)**  **, peanut , potato,**  **pepper/eggplant subgroup 8** 
**- 10B,**  **melon subgroup 9A , soybeans,**  **imported wine grapes and sherry and resulting secondary residues in meat and milk** **. For acute dietary exposure, the acute population adjusted dose (aPAD) was based on the NO**  **A EL of 50 m**  **g/kg bw/day from an acute rat neurotoxicity study.**  **For females 13**
**- 49 years of age, the**  **NOAEL of 7 mg/kg bw/day from the rabbit developmental toxicity study was used for acute dietary exposure.**  **Fo r chronic dietary exposure, the chronic population**  **adjuste d dose (cPAD) was based on the NO**  **A EL from the**  **mouse carcinogenicity study (1**  **.1 mg/kg bw/day). An uncertainty factor of 100 was used in both cases since**  **the results of a DNT study confirmed there was no increased sensitivity of the fetus**6

**or young rat pups to fluazinam as compared to the dams and the FQPA uncertainty**  **factor could be reduced to one (1) .**  i. Food. **Acute Risk Tier 1 acute dietary exposure analyses were conducted for fluazinam to determine the exposure contribution of**  **the above mentioned comm**  **odities to the diet and to ascertain the acute risk potential. The estimates were based on: proposed tolerance level residues for all the crops; apple, peanut and**  **potato processing studies; market share assumptions of 100% crop treated (except wine grapes**  **where it was assumed that 100% of the imported wine grapes would be treated and 39% of wine consumed in the US is imported);**  **screening**
**- level acute**  **EDWC of 218 ppb for water**  **; and consumption data from USDA’s CSFII (1994**  **through 1998) continuing survey of f ood intake.**  **Even using all of the worst**
**- case exposure scenarios listed above, the Tier 1 95th**  **percentile acute dietary exposure (per capita) fr**  **om food and drinking water**  **for the U.S. population was estimated to**  **be 0.0 24402**  **mg/kg bw/day or 4.9**  **% of the a**  **PAD. The highest acute exposure estimate (95th percentile) was observed in the females**  **13**
**- 49 yrs.**  **subpopulation: 0.01 8334**  **mg/kg bw/day. This corresponds to 26.1**  **% of**  **the aPAD. Chronic Risk Tier 1 dietary exposure analyses were conducted for fluazinam**  **to determine the exposure**  **contribution of th e above mentioned**  **commodities to the diet and to ascertain the chronic risk potential. The estimates were based on: proposed**  **tolerance level residues for all the crops , accept apples where average field resi**  **d ue**  **s were**  **used ; apple, peanut and potato processing studies; market share assumptions**  **of 100% crop treated (except wine grapes where it was assumed that 100% of the imported wine grapes would be treated and 39% of wine consumed in the US is**  **imported); screening** 
**- level chronic EDWC of**  **37 ppb;**  **and consumption data from USDA’s CSFII (1994 through 1998) continuing survey of food intake.**  **Even using all of the worst**
**- case exposure scenarios listed above, the Tier 1**  **chronic dietary exposure estimates resulted in an e stimated exposure for the U.S.**  **population of 0.001 924**  **mg/kg bw/day. This exposure corresponds to 1 7.5**  **% of the cPAD of 0.011mg/kg bw/day. The highest exposure estimate was calculated for the**  **all infants (<1 year) population subgroup. This exposure was de termined to be**  **0.00 5609**  **mg/kg bw/day (51.0**  **% of the cPAD) most**  **of which was due to the water contribution**  **. It can be concluded that acute or long**  **- term dietary exposure to fluazinam**  **through residues on treat ed apple, carrot,**  **brassica (cole) leafy vegetab les (Group 5)**  **including turnip greens, bean (Groups 6A, 6B and 6C), bushberry (Group 13**
**- 07B),**  **ginseng, head lettuce, leaf lettuce, bulb onion (Crop 3**
**- 07A), peanut, potato,**  **pepper/eggplant subgroup 8**
**- 10B, melon subgroup 9A, soybeans,**  **imported wine grapes a**  **nd sherry should not be of cause for concern.** ii. Drinking water

. **Since fluazinam is intended for application outdoors to field grown crops, the potential exists for parent and** **/ or metabolites to reach ground**  **or surface water that may be used for drinki ng water. The potential estimated**  **drinking water concentrations (EDWCs) associated with the application of fluazinam to**  **soybeans, is less than the maximum values estimated for**  **turf . Thus,** 7

**the more conservative**  **screening**
**- level acute EDWC (218 ppb) and chr**  **onic EDWC (37 ppb)**  **for turf**  **were incorporated into the DEEM** 
**- FCID model to estimate dietary**  **exposure .**  2. Non

- dietary exposure

. **A registration**  **f or the use of**  **fluazinam on golf**  **courses is**  **pending .**  **Applications are to be made by golf course workers only** **, thus**  **no residential handler exposure is expected .**  **However, post** **- application**  **dermal exposure from contact with the treated turf on golf courses may occur. Thus, post** 
**** **application dermal exposure was calculated for adults and**  **for youth playing golf**  **, using t** **he general US population subgroup and**  **youth , 13** 
**- 19 years**  **subgroup . T**  **he Margins of Exposure (MOE) for both**  **the adults (21,800) and**  **the youth (14,300)**  **were well above the acceptable MOE of 100.** D. Cumulative Effects **Fluazinam is a phenylpyridinyla mine fungicide. Since there are no other**  **members of this class of fungicides, it is considered unlikely that fluazinam would have a common mechanism of toxicity with any other pesticide in use at this time**  **.** E. Safety Determination 1. U.S. population. **Dietary and**  **post -**  **application dermal**  **exposure from**  **recreational contact**  **with treated**  **turf on**  **golf courses**  **will be**  **the routes**  **of exposure**  **to the**  **U.S. population.**  **Am ple**  **margins of**  **safety have**  **been demonstrated**  **for both**  **situations. For**  **the general**  **U.S. po**  **pulation, the**  **chronic aggregate**  **risk assessment**  **is based**  **on exposure**  **from food**  **a nd**  **drinking water**  **only, since**  **no residential**  **uses exist.**  **A s**  **noted above,**  **the chronic**  **dietary exposure**  **to fluazinam**  **represents 17.5**  **% of**  **the cPAD**  **for the**  **overall U.S.**  **population ,**  **using the**  **conservativ e**  **Tier I**  **assumptions .**  **A cancer**  **dietary assessment**  **was not**  **conducted because**  **this product**  **has been**  **classified as**  **“ suggestive**  **evidence of**  **carcinogenicity, but**  **not sufficient**  **to assess human carcinogenic potential**  **.” An**  **acute aggregate**  **risk assessment**  **is required**  **for the**  **general population**  **and for**  **the subgroup**  **of females**  **13**
**- 49**  **years old.**  **For both**  **of these**  **population s**  **, the**  **acute dietary**  **(food and**  **drinking water)**  **risk assessment**  **represents acute**  **aggregate risk**  **since the**  **dietary route**  **alon e**  **is relevant**  **for acute**  **exposure and**  **risk assessment.**  **As noted**  **above, the**  **acute dietary**  **exposure to**  **fluazinam is**  **estimated to**  **be 4.9%**  **of the**  **aPAD for**  **the overall**  **U.S. population,**  **and 26.1%**  **of the**  **aPAD for**  **the subgroup**  **of females**  **13**
**- 49**  **years old.**  **These valu**  **es were**  **presented above**  **and are**  **below the**  **Agency’ level of concern. Short** 
**- term**  **and intermediate** 
**- term**  **aggregate risks**  **include chronic**  **dietary and**  **short -** **term residen**  **tial sources**  **of exposure.**  **Since Fluazinam**  **is proposed**  **for use**  **on golf**  **courses there**  **is pote**  **ntial for**  **post -**  **application exposure**  **to adults**  **and youths**  **from playing**  **golf. T**  **he US**  **general population**  **was chosen**  **as the**  **representative short** **- term**  **population for**  **adults, while**  **the dietary**  **subpopulation youths**  **aged 13**  **to**8

**19 was**  **chosen to**  **match with**  **the yout** **h golfer**  **residential exposure.**  **The d**  **ietary (food**  **and drinking**  **water) exposure**  **was based**  **on the**  **Tier I**  **chronic exposure**  **assessment as**  **noted above**  **but converted**  **to an**  **MOE .**  **This was aggregated**  **with the**  **appropriate post**
**- application residential golfer MOE to**  **yield the following aggregate short/intermediate** 
**- term**  **MOEs: US**  **general population**  **MOE =**  **1811; youths,**  **13**
**- 19**  **= 2779.**  **T hese**  **aggregate risks**  **are well**  **above 100**  **for all**  **populations, indicating**  **acceptable risks for both adults and youth. Based on this infor**  **mation, it can be concluded that there is reasonable certainty that no**  **harm will**  **result from**  **acute ,**  **short/intermediate term**  **or chronic**  **exposure to**  **fluazinam .**  2. Infants and children

. **Data from developmental toxicity studies in the rat and rabbit, a 2** 
**- g**  **eneration reproduction study and a developmental neurotoxicity study were considered. These studies,**  **that were described earlier, demonstrated no**  **increased sensitivity of rats or rabbits to in utero or gavage exposure of pups to fluazinam. In addition, t** **he multigeneration reproductive toxicity study did not identify any increased sensitivity of rats to in utero or postnatal exposure. For all**  **four studies, parental NOAEL**  **s were lower than or equivalent to the developmental or offspring**  **NOAEL s. It is concl**  **uded that the standard margin of safety will protect the safety of infants and children and that an additional FQPA safety factor**  **is not warranted. The dietary exposure of fluazinam to infants and children is estimated to be**  **less than any level of con**  **cern . The proposed tolerances**  **plus drinking water input will**  **utilize 20.5**  **% of the aPAD**  **for the “Children (1** 
**- 2 years)”**  **subgro up,**  **and 51.0**  **% of the**  **cPAD for the**  **“All I nfants (<1 year)**  **“ subgroup.**  **(These were the most sensitive infant/child subgroups**  **. )**  **Thus, i t can be concluded that there is reasonable certainty**  **that no harm will result to infants and children from acute or chronic exposure to fluazinam**  **.]** F. International Tolerances **[ There are presently no Codex maximum residue levels (MRLs) established**  **for residues of fluazinam on any crop. The Canadian established MRLs for**  **brassicas (crop group 5A & 5B), bushberries (crop group 13B), dry beans, lima beans, snap beans, and the**  **Mexican MRLs for beans and potatoes are similar to the**  **tolerances established for these crops in the USA**  **.]**