


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

EPA Registration Division contact: [Mike Goodis, RD]

Makhteshim Agan of North America, Inc. 

PP# 8F8719

EPA has received a pesticide petition (PP# 8F8719) from Makhteshim Agan of North America, Inc. (d/b/a ADAMA), 3120 Highwoods Blvd, Suite 100, Raleigh, NC 27604  requesting to: 1) amend the tolerance expression in 40 CFR 180.680 paragraphs (a) and (d) to read "Tolerances are established for residues of the nematicide fluensulfone, including its metabolites and degradates, in or on the commodities in the table below. Compliance with the tolerance levels specified in the following table below is to be determined by measuring only the sum of fluensulfone, 5-chloro-2-[(3,4,4-trifluoro-3-buten-1-yl)sulfonyl]thiazole and its metabolite, 3,4,4‐trifluoro‐but‐3‐ene‐1‐sulfonic acid, calculated as the stoichiometric equivalent of fluensulfone, in or on the commodity"; and, 2) to amend the tolerances in 40 CFR 180.680 for residues of the nematicide, fluensulfone and its metabolite BSA expressed as fluensulfone equivalents, on the raw agricultural commodities as follows: Fruit, pome, group 11 at 0.4 parts per million (ppm);  Fruit, stone, group 12 at 0.1 parts per million (ppm); Fruit, small vine climbing subgroup 13-07D at 0.8 parts per million (ppm); Nut, tree, group 14 at 0.04 parts per million (ppm); Almond hulls at 5 parts per million (ppm); Sugarcane at 0.05 parts per million (ppm); Molasses at 0.3 parts per million (ppm); and,
  *   rotated cereal grains (inadvertent residues with 10-month PBI): Grain, cereal, group 15 at 0.05 parts per million (ppm); and Grain cereal, forage, fodder and straw, group 16 at 3 parts per million (ppm); and,
  *   rotate wheat (inadvertent residues with 90-day PBI): Wheat grain (includes triticale) (Barley grain; Buckwheat grain; Oat grain; and Teosinte grain) at 0.1 parts per million (ppm); Wheat bran (Barley bran) at 0.14 parts per million (ppm); Wheat middlings at 0.10 parts per million (ppm); Wheat shorts  at 0.11 parts per million (ppm); Wheat germ at 0.10 parts per million (ppm);  Wheat straw (Barley straw and Oat straw) at 6 parts per million (ppm);  Wheat forage (Oat forage) at 6  parts per million (ppm); and, Wheat hay (Barley hay and Oat hay) at 15 parts per million (ppm).

The purpose of proposing these amended tolerances/MRLs is to harmonize the EPA, PMRA, and JMPR tolerance residue definitions.  Note that EPA published a Notice of Filing for PP# 7F8650 on May 18, 2018 which proposed the harmonization of the existing tolerances for fluensulfone under the new tolerance expression.  The notice herein proposes harmonization of all of the remaining tolerances for fluensulfone, including new tolerances established beyond the point at which they could have been incorporated into the May 18, 2018 notice.

  
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.  Fluensulfone is supported by a complete plant metabolism data package. In all plant matrices, whether from a primary or rotational crop, a clear pattern was observed with TSA (M-3625) and BSA (M-3627) forming the majority of the residues following the cleavage of fluensulfone.  Both compounds have lower acute oral and subchronic toxicity than parent fluensulfone and neither shows any genotoxic potential in a range of mutagenicity studies.  As mentioned above, the proposed tolerance residue definition is parent fluensulfone plus its metabolite 3,4,4-trifluoro-but-3-ene-1-sulfonic acid (BSA) expressed as fluensulfone equivalents.  The existing risk assessment residue definition of fluensulfone expressed as fluensulfone will remain unchanged. 

	2. Analytical method. Adequate analytical methods for determining fluensulfone in/on appropriate raw agricultural commodities and processed commodities have been developed and validated, including LC-MS/MS methods.  The analytical procedures have been successfully validated in terms of specificity, linearity, precision, accuracy and LOQ.  

      The MRM study demonstrates that the FDA multiresidue methods (MRMs) are not suitable for detection and enforcement of fluensulfone residues as sulfonic acid metabolites in non-fatty matrices.

	3. Magnitude of residues. Fluensulfone is registered for use on a variety of crop groupings and an extensive residues package has been generated at field trial sites in the USA and Canada.  Fluensulfone and M-3627 (BSA) were sought in all samples. The LOQ is 0.01 mg/kg. The generated data supports the amended tolerances proposed in this document. 

Adequate data are available to propose tolerances (MRLs) and there is no unacceptable risk to consumers from the consumption of crops treated with formulations containing fluensulfone.

B. Toxicological Profile

      1. Acute toxicity.  The acute oral LD50 is 671 mg/kg bw in rats.  The acute dermal LD50 of fluensulfone is >2000 mg/kg bw.  The acute inhalation LD50 in rats is >5.1 mg/L.  Fluensulfone displayed no eye irritation in rabbits.  Fluensulfone is not irritating to the skin and is a skin sensitizer.  

      2. Genotoxicty. A complete data package of in vitro and in vivo mutagenicity studies is available for fluensulfone.  A full summary of the genotoxicity database is provided in the OECD Dossier.  On the basis of the robust in vitro and in vivo mutagenicity data, it is concluded that fluensulfone does not possess any genotoxic potential.

      3. Reproductive and developmental toxicity. The reproductive toxicity of fluensulfone was evaluated in a 2-generation reproduction study in rats. Developmental toxicity was assessed in rats and rabbits.  

      Reproductive toxicity.  A 2-generation reproduction study in rats was conducted at dose levels of 0, 30, 250 and 1800 ppm (2.0, 16.2, and 122.0 mg/kg/day in males and 2.8, 23.0 and 169.1 mg/kg/day in females).  Treatment with fluensulfone up to and including 1800 ppm, the highest tested dose level, showed no effects on reproductive function, including gonadal function, mating behavior, fertility, viability of offspring, breeding, conception, gestation and parturition. 
      
      Parental systemic toxicity was evident however, with effects on body weight development throughout the study observed at 1800 ppm (the LOAEL); hence the NOAEL was set at 250 ppm (equivalent to approximately 16.2 mg/kg/day in males and 23.0 mg/kg /day in females). A NOAEL for general toxicity in F1 and F2 pups was established at 250 ppm, based on reduced pup weight noted at 1800 ppm.
      
      Developmental toxicity.  Fluensulfone was not teratogenic or fetotoxic either in rats or rabbits. 
      
      A pre-natal developmental study in rats included dose groups of 0, 7.7, 48.6, and 292.0 mg/kg/day.  Maternal toxicity, manifested as decreased body weight gain and food consumption in rats, resulted in a lower body weight of female pups; the maternal and developmental NOAEL was set at 48.6 mg/kg/day.
      
      A pre-natal developmental study in rabbits included dose groups of 0, 2.5, 10 and 40 mg/kg/day.  Similarly, as with the study in rats, treatment of rabbits at 40 mg/kg/day resulted in slight maternal toxicity consisting of reduction in food consumption at the onset of the treatment and between days 18 and 24, and reduced mean body weight gain at the beginning of the treatment only. As the lower fetal weights recorded at this dose level were within the range of the historical control data, the NOAEL for maternal and developmental toxicity was considered to be 40 mg/kg/day, the highest dose tested.

      4. Subchronic toxicity. Repeated dose, oral (dietary) toxicity studies with fluensulfone are available for rats, mice and dogs.  The studies conducted include 28-day and 90-day studies in the rat, mouse, and dog.  In addition, a 1-year oral toxicity study in dogs and a 28-day dermal toxicity study in rats were performed.

The rat 28-day study was conducted at dose levels of 0, 125, 500, and 2000 ppm (0, 10.4, 42.5, and 152 mg/kg/day in males and 0, 12.2, 37.2, and 165.9 mg/kg/day in females).  The NOAEL was 125 ppm (10.4 and 12.2 mg/kg day in males and females respectively), based on results at the LOAEL of functional effects in the liver and kidney effects, which were considered adverse as a precaution but likely of no toxicological relevance.

The mouse 28-day study was conducted at dose levels of 0, 100, 500, and 2000 ppm (0, 30.33, 101.31, and 374.5 mg/kg/day in males and 0, 41.32, 155.12, and 353.0 mg/kg/day in females).  The NOAEL was 100 ppm (30.33 and 41.32 mg/kg/day in males and females respectively), based on results at the LOAEL of decreased food consumption and liver toxicity (increased relative weight, histopathological findings).  

The dog 28-day study was conducted at dose levels of 0, 50, 200, and 900 ppm (1.9, 7.3, and 30.9 mg/kg/day in males and 2.0, 7.9, and 29.7 mg/kg/day in females).  The NOAEL was 200 ppm (7.3 and 7.9 mg/kg/day in males and females respectively), based on results at the LOAEL of slight changes in food consumption, body weight and organ weight (liver and thyroid) and on hepatic tissue enzyme activities. 

The rat subchronic 90-day study was conducted at dose levels of 0, 60, 120, 500 and 2000 ppm (4.31, 8.26, 34.86, and 139.01 mg/kg/day in males and 4.85, 11.68, 53.10 and 148.73 mg/kg/day in females).  The NOAEL was 120 ppm (8.3 and 11.7 mg/kg/day in males and females respectively), based on results at the LOAEL of decreased body weight/body weight gain in males, increased water consumption in males and increased triglycerides in females.  

The mouse subchronic 90-day study was conducted at dose levels of 0, 60, 300, and 1500 ppm (11.06, 50.85, and 228.53 mg/kg/day in males and 18.33, 68.47 and 252.49 mg/kg/day in females).  The NOAEL was 60 ppm (11.06 and 18.33 mg/kg/day in males and females, respectively), based on results at the LOAEL of decreased food consumption in females and marginal effects in liver and hematological findings in males.    

The dog subchronic 90-day study was conducted at dose levels of 0, 5, 50, and 500 ppm (0.2, 1.6 and 17.1 mg/kg/day in males and 0.2, 1.8 and 18.0 mg/kg/day in females).  The NOAEL was 500 ppm (17.1 and 18.0 mg/kg/day in males and females, respectively), based on only slight and reversible liver effects at the top dose tested.  

The rat 28-day dermal study was conducted at dose levels of 0, 80, 400, and 2000 mg/kg/day in males and females.  Only a minimal increase in the incidence of acanthosis/hyperkeratosis was observed at the limit dose of 2000 mg/kg/day.  However, because of the moderate degree recorded in comparison to the vehicle control, the finding was considered adaptive and likely to be reversible after cessation of treatment and on this basis not adverse. The NOAEL was 2000 mg/kg/day, the highest dose tested, based on no systemic or adverse dermal effects at the highest dose level tested.

In all species the liver appears to be the main target organ, although often the observed effects were limited to adaptive changes (e.g. hepatocyte hypertrophy concomitant to increased weight, induction of mainly phase II activities). Investigations on liver enzyme activities in all species revealed that fluensulfone administration does not result in significant induction of (activating) phase I cytochrome P450 subfamilies, but that the (conjugating) phase II enzymes were induced. Frank hepatotoxicity was observed only at very high doses, and only in mice.

The NOAEL for oral subchronic toxicity is 8.3 mg/kg bw/day based on decreased body weights in males (and supported by increased triglycerides in females at the same dietary dose) in the 90 day rat study. The NOAEL for dermal subchronic toxicity is 2000 mg/kg bw/day, based on absence of adverse effects at the highest test dose in the rat 28-day dermal toxicity study.

      5. Chronic toxicity. The long-term toxicity and carcinogenicity potential of fluensulfone was evaluated in dogs (one year study), rats (combined study for chronic toxicity and carcinogenicity), and mice (carcinogenicity). 
      
In a 1-year oral toxicity study in dogs, fluensulfone was administered in the diet at 0, 5, 50 100 and 500 ppm (0.1, 1.5, 3.1, and 19 mg/kg/day in males and 0.1, 1.5, 3.3, and 16.2 mg/kg/day in females) to purebred Beagle dogs for a period of 52 weeks with selected animals retained for an 8-week recovery period.  The NOAEL was considered to be 100 ppm (3.1 mg/kg bw/day in males and 3.3 mg/kg bw/day in females), based on decreased body weight and body weight gains, decreased hemoglobin, MCH, MCHC and increased kidney weights at 500 ppm (16.0 and 16.2 mg/kg/day in males and females respectively) in the diet.
A combined chronic dietary toxicity and carcinogenicity study in rats was conducted with 0, 30, 200, and 1200 ppm dose groups (1.6, 11 and 66.3 mg/kg/day after 52 weeks and 1.4, 9.6 and 57.7 mg/kg/day after 104 weeks in males; 1.9, 13.1 and 75.2 mg/kg/day after 52 weeks and 1.7, 11.6 and 69.3 mg/kg/day after 104 weeks in females). Fluensulfone showed no carcinogenic potential in this study, and the NOAEL for lifespan treatment (2-years) was set at 30 ppm (1.4 mg/kg/day in males and 1.7 mg/kg/day in females) on the basis of chronic interstitial inflammation in the lungs of females, decreased body weight and body weight gain in males, and decreased hemoglobin concentration and hemoglobin concentration distribution width in females receiving 200 ppm.
      
A 78-week dietary carcinogenicity study in mice was conducted with 0, 30, 200, and 1200 ppm dose groups (4.2, 27.6 and 152.3 mg/kg/day in males and 6.4, 39.0, and 188.4 in females).  The overall NOEL in mice following lifespan treatment was set at 30 ppm (4.2 and 6.4 mg/kg/day in males and females, respectively). In mice, treatment with fluensulfone for 78 weeks resulted in an increased incidence of alveolar/bronchiolar adenomas in females receiving 200 and 1200 ppm. Mechanistic studies were carried out to determine the relevance for humans of this finding. Tumors were found to be a species-specific effect in mice due to activation of fluensulfone by mouse lung Clara cells, leading to local cytotoxicity, cell proliferation and finally formation of benign tumors.  Rats have lower metabolic activity in the lungs compared to mice (below the threshold needed to cause lung tumors upon lifetime exposure) and activity in humans is orders of magnitude lower than rats.  Fluensulfone was found to be extensively metabolized by mouse lung microsomes, whereas no metabolic activity was seen in human lung microsomes.    In accordance with the International Programme on Chemical Safety (IPCS) mode of action and human relevance framework, it is concluded that fluensulfone leads to species-specific tumors via a non-genotoxic threshold mode of action in the mouse lung, and that these tumors are not relevant to human hazard or risk.

The NOAEL for lifespan treatment was set at 1.4 mg/kg/day on the basis of decreased body weight and body weight gain in males (supported by chronic interstitial inflammation in the lungs and decreased hemoglobin concentration and hemoglobin concentration distribution width in females).

      6. Neurotoxicity. Acute and subchronic specific neurotoxicity studies (i.e. inclusive of neuropathology) were carried out, and functional observation batteries (FOBs) and motor activity assessments were included in the repeated dose/chronic studies with fluensulfone.  The FOBs and motor activity assessments conducted within the repeated dose/chronic toxicity studies revealed no effects.
      
In an acute oral neurotoxicity study in rats, groups of 10 male and 10 female Wistar rats were administered single oral doses of 0 (control), 100, 400 and 1200 mg/kg bw of fluensulfone by oral gavage  and observed for 14 days.  No test item-related effects on absolute and relative brain weights were evident, and there were no findings in the nervous system during macroscopic and microscopic pathology examinations.  The LOAEL for general toxicity is 100 mg/kg bw in males and females, based on the general systemic toxicity due to the bolus dose.  The NOAEL for neurotoxicity is 100 mg/kg bw in males and females, based on reduced activity in the functional observation battery and decreased motor activity at 400 mg/kg in absence of any neuropathological finding at any dose level.
      
In a subchronic dietary neurotoxicity study, groups of 12 male and 12 female RccHan:WIST (SPF) rats received fluensulfone in their diet at concentrations of 0 (control), 100, 500 and 2500 ppm (0, 6, 31, and 153 mg/kg/day in males and 0, 7, 34, and 162 mg/kg/day in females) for at least 90 days.  Treatment-related effects were confined to lower food consumption, body weight and body weight gain in males and females at 2500 ppm. These treatment-related effects were attributed to systemic toxicity, and not to neurotoxicity.  No effects on functional parameters or neurohistopathology were observed. Therefore, the high dose level of 2500 ppm was the `no-observed-effect level' (NOEL) for neurotoxicity associated with dietary exposure, equivalent to 153 mg/kg bw/day in males and 162 mg/kg bw/ day in females.  The no-observed-adverse-effect level (NOAEL) for systemic toxicity was 500 ppm equivalent to 31 mg/kg bw/day for males and 34 mg/kg bw/day for females. 
      
As developmental studies did not indicate that the offspring are more sensitive than the adult, and neuropathological effects were not observed in any of the performed neurotoxicity studies, a developmental neurotoxicity study was considered not necessary.

      7. Immunotoxicity.  Although immunotoxicity endpoints were already included in the 28-day dietary study in rats and mice, fluensulfone was tested also in mice in the 28-day sheep red blood cell assay, to evaluate its immunotoxicity potential. In addition, the entire available data set was examined to check immunotoxicity-related endpoints.  It is concluded that fluensulfone is not an immunotoxic substance.
      
      8. Animal metabolism. Fluensulfone (labeled at the thiazole and the butene-moieties of the molecule) administered orally to rats at nominal single doses of either 5 mg/kg or 500 mg/kg is rapidly metabolized. The recovery of radioactivity was essentially complete for all groups of rats. The disposition and excretion of radiolabel for males and females were generally similar. There was no indication that the metabolic elimination processes were saturated by the 100-fold increase in dose level, as levels of radiolabel in urine, cage wash, feces, carcass, and gastro-intestinal (GI tract) were similar. 

Urine was the major route of excretion and the only source of metabolites at >=5% of the applied radiolabel.  The cage wash contained relatively high levels of radiolabeled metabolites and analysis showed that those metabolites in cage wash and urine were similar.  Low amounts of thiazole sulfonic acid were found in feces, but no other fecal metabolites were >=5% of the applied dose.  Fluensulfone is not a significant residue in either urine or feces.  

In addition to investigating metabolism after a single dose, the tissue distribution was studied when the dosing of radioactivity was preceded by 14 days administration of unlabelled material.  The results indicate that distribution is comparable in both cases.

	9. Metabolite toxicology. The acute oral LD50 of fluensulfone metabolite M-3625 (TSA) was greater than 2000 mg/kg(less than that of the parent fluensulfone).  

Metabolite M-3625 was tested for its genotoxic potential in a bacterial reverse gene mutation assay, an in vitro chromosome aberration assay in mammalian cells, and an in vivo micronucleus assay in the bone marrow of rat. No genotoxic properties were identified.

In a 90-day dietary repeated dose study with Metabolite M-3625 in rats, no adverse effects were reported at the highest dose tested (12,000 ppm), which is equivalent to 975/1369 mg/kg/day in males/females, respectively.

      The acute oral LD50 of fluensulfone metabolite M-3627 (BSA) was greater than 2000 mg/kg bw (less than that of the parent fluensulfone). 

Metabolite M-3627 was tested for its genotoxic potential in a bacterial reverse gene mutation assay, an in vitro chromosome aberration assay in mammalian cells, and an in vivo micronucleus assay in the bone marrow of rat. No genotoxic properties were identified.

In a 90-day dietary repeated dose study with Metabolite M-3627 in rats, no adverse effects were reported at the highest dose tested (11,000 ppm), which is equivalent to 851/974 mg/kg/day in males/females, respectively.

	10. Endocrine disruption. Evidence from the large available toxicological data set demonstrates that fluensulfone does not exert any adverse effects on thyroid gland, reproductive system and related endocrine organs and adrenal glands.  Therefore, it is concluded that fluensulfone does not possess any endocrine disrupting potential.

C. Aggregate Exposure

	1. Dietary exposure. As this document only petitions for a change in EPA's current tolerance residue definition, EPA's existing dietary risk assessment residue definition will remain unchanged and therefore no additional dietary risk assessments were conducted.  Therefore, the dietary risk assessment (MRID# 50340502) included in the petition submitted to EPA on August 24, 2017 is still valid and the results from that assessment are presented here.  Acute and chronic dietary (food + water) exposures to fluensulfone have been estimated for proposed and existing uses. The recent drinking water modeling conducted by EPA (2016, DP Barcode D432134) is still relevant and results were incorporated into the assessment. It been determined that MMPE does not need to be included in the dietary exposure and risk assessment.  A Tier 1 acute dietary exposure assessment was conducted assuming tolerance-level residues, 100% crop treated and default processing factors. Exposure was assessed using the acute and chronic toxicological endpoints determined by EPA (2016. DP Barcode D432134), which are an aPAD of 0.16 mg/kg bw/day derived from a NOAEL of 16.2 mg/kg bw/day from a 2-generation reproduction rat study and a cPAD of 0.10 mg/kg bw/day derived from a NOAEL of 9.6 mg/kg bw/day from a 2-year toxicity/carcinogenicity rat study.  EPA has determined that the level of concern for fluensulfone for acute and chronic exposures is 100 (EPA, 2016, DP Barcode D432134).

      Acute Dietary Exposure.  Acute dietary (food + water) exposures to fluensulfone, were calculated using DEEM- FCID version 4.02. The reported exposures correspond to the 95th percentile of the exposure distributions, as is appropriate for a Tier 1 acute dietary exposure assessment. The 95th percentile acute dietary (food + water) exposures are well below the aPAD (0.16 mg/kg/d). For all infants, the most highly exposed subpopulation, 95th percentile acute dietary exposures correspond to 9.90% of the aPAD. For the general U.S. Population, 95th percentile acute dietary exposures correspond to 3.08% of the aPAD. Acute dietary exposures below 100% of the aPAD are reasonably anticipated to result in no harm to exposed populations.
      
      Chronic Dietary Exposure.  Chronic dietary exposures to fluensulfone were calculated using DEEM-FCID version 4.02.  The chronic dietary exposures are less than the cPAD (0.10 mg/kg/d). For infants, the most highly exposed subpopulation, chronic dietary exposures correspond to 5.1% of the cPAD.  For the general U.S. Population, chronic dietary exposures correspond to 1.4% of the cPAD. Chronic dietary exposures below 100% of the cPAD are reasonably anticipated to result in no harm to exposed populations.
      
	i. Food. Exposure to fluensulfone through food is included in the dietary assessment section above.  

	ii. Drinking water. Exposure to fluensulfone through water is included in the dietary assessment section above.  

	2. Non-dietary exposure. No new residential uses are being proposed.  The aggregate exposure incorporating the estimated dietary exposures from the currently registered and proposed crop uses and EPA's existing total residential exposures for the turf use do not result in unacceptable exposure or risk. 

D. Cumulative Effects

	Fluensulfone is a member of a new chemical class of nematicides with a specific toxicological profile. It does not share a known toxicological mode of action with other pesticides. Thus, no cumulative effects are foreseen.


E. Safety Determination

1. U.S. population. Using the conservative exposure assumptions described above and based on the completeness of the toxicity data, it can be concluded that total food and drinking water exposure to fluensulfone from all proposed crop uses will be 3.08% of the aPAD and 1.4% of the cPAD for the overall US population.

2. Infants and children. Using the conservative exposure assumptions described above and based on the completeness of the toxicity data, it can be concluded that the total acute food and drinking water exposure to fluensulfone from all proposed crop uses will be 9.90% (all infants), 4.96% (children 1-2 yrs), 4.23% (children 3-5 yrs), and 2.94% (6-12 yrs) of the aPAD. It can be concluded that the total chronic food and drinking water exposure to fluensulfone from all proposed crop uses will be 5.1% (all infants), 2.5% (children 1-2 yrs), 2.0% (children 3-5 yrs), and 1.3% (children 6-12 yrs) of the cPAD.

F. International Tolerances

Codex MRLs for the crops mentioned herein:  Beetroot (4 ppm), Brassica (Cole or Cabbage) Vegetables, Head Cabbage, Flowerhead Brassicas (1.5 ppm), Carrot (4 ppm), Celeriac (4 ppm), Celery (2 ppm), Chervil, Turnip-rooted (4 ppm), Cucumber (0.7 ppm), Fruiting vegetables other than cucurbits (except sweet corn and mushrooms) (0.7 ppm), Horseradish (4 ppm), Komatsuma (9 ppm), Leafy vegetables not specified elsewhere (1 ppm),  Legume Vegetables (0.1 ppm). Lettuce, Head (0.8 ppm), Low growing berries (0.5 ppm), Melons, except watermelon (0.3 ppm), Mustard Greens (20), Parsnip (4 ppm), Peppers, chili, dried (7 ppm), Potato (0.8 ppm), Potato, dried (2 ppm), Radish (4 ppm), Radish leaves, including radish tops (50 ppm), Radish, Japanese (4 ppm), Root and tuber vegetables not specified elsewhere (3 ppm), Spinach (4 ppm), Squash, summer (0.7 ppm), Swede (4 ppm), Sweet potato (0.8 ppm), Tomato paste (1,5 ppm), Tomato, dried (1.5 ppm), Turnips greens (10 ppm), Turnips, garden (4 ppm), and Watermelon (0.3 ppm).

Canadian MRLs for the crops mentioned herein: Fruiting vegetables (CG 8-09; except small tomatoes) (0.5 ppm), Tomato paste (1 ppm), Vegetables, cucurbits, group 9 (0.6 ppm).


	 

