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Federal Register / Vol. 86, No. 44 / Tuesday, March 9, 2021 / Rules and Regulations
and authorized under FFDCA section 408f1. Data will be required to be submitted no later than 5 years from the date of issuance of these tolerances.
EPA did not use information on the percent of food actually treated in the dietary assessment for fluindapyr; 100
PCT was assumed for all food commodities.
2. Dietary exposure from drinking water. The Agency used screening level water exposure models in the dietary exposure analysis and risk assessment for fluindapyr in drinking water. These simulation models take into account data on the physical, chemical, and fate/
transport characteristics of fluindapyr.
Further information regarding EPA
drinking water models used in pesticide exposure assessment can be found at http www2.epa.gov/pesticide-scienceand-assessing-pesticide-risks/aboutwater-exposure-models-used-pesticide.
Using the Pesticide Water Calculator PWC, version 1.52, the estimated drinking water concentrations EDWCs of fluindapyr were determined to be higher in groundwater than in surface water for both acute and chronic exposure durations. The following groundwater EDWCs were used directly in the dietary exposure model to account for the contribution of fluindapyr and relevant transformation products 3OHF9990 and 1COOH
F9990 residues in drinking water as follows: 254.1 ppb was used in the acute assessment and 217.8 ppb was used in the chronic assessment.
3. From non-dietary exposure. The term residential exposure is used in this document to refer to nonoccupational, non-dietary exposure e.g., for lawn and garden pest control, indoor pest control, termiticides, and flea and tick control on pets.
Fluindapyr is currently registered for the following use that could result in residential exposures: Golf course turf.
The currently registered use on golf courses will result in short-term 1 to 30
days residential post-application dermal exposures to adult, youth 11 to less than 16 years old, and children 6
to less than 11 years old. Further information regarding EPA standard assumptions and generic inputs for residential exposures may be found at http www.epa.gov/pesticides/trac/
science/trac6a05.pdf.
4. Cumulative effects from substances with a common mechanism of toxicity.
Section 408b2Dv of FFDCA
requires that, when considering whether to establish, modify, or revoke a tolerance, the Agency consider available information concerning the cumulative effects of a particular pesticides residues and other
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substances that have a common mechanism of toxicity.
Unlike other pesticides for which EPA
has followed a cumulative risk approach based on a common mechanism of toxicity, EPA has not made a common mechanism of toxicity finding as to fluindapyr and any other substances and fluindapyr does not appear to produce a toxic metabolite produced by other substances. For the purposes of this action, therefore, EPA has not assumed that fluindapyr has a common mechanism of toxicity with other substances.
D. Safety Factor for Infants and Children 1. In general. Section 408b2C of FFDCA provides that EPA shall apply an additional tenfold 10X margin of safety for infants and children in the case of threshold effects to account for prenatal and postnatal toxicity and the completeness of the database on toxicity and exposure unless EPA determines based on reliable data that a different margin of safety will be safe for infants and children. This additional margin of safety is commonly referred to as the FQPA Safety Factor SF. In applying this provision, EPA either retains the default value of 10X, or uses a different additional safety factor when reliable data available to EPA support the choice of a different factor.
2. Prenatal and postnatal sensitivity.
In the developmental toxicity studies rat and rabbit, fluindapyr did not produce any adverse effects in parental animals or fetuses at or approaching the limit dose 1,000 mg/kg/day. In the reproduction study, in parental animals P and F1 males and females, fluindapyr induced an increase in thyroid follicular hypertrophy/
hyperplasia. It also induced adverse effects on a host of reproductive parameters. There is no evidence of increased quantitative or qualitative susceptibility in the developmental toxicity studies in rabbits or rats or the reproductive toxicity study in rats. In the 2-generation reproduction study in rats, reproductive effects were observed, and offspring toxicity decreased pup weights in F1 and F2 generation;
thymus and spleen weights were decreased was observed in the presence same dosage of parental toxicity increase in thyroid follicular hypertrophy/hyperplasia and reproductive effects.
3. Conclusion. Due to the uncertainties concerning the potential life stage susceptibility related to adverse thyroid effects seen in parental animals of the reproductive study, EPA
is retaining the FQPA 10X SF for
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exposure scenarios that rely on the reproductive study in which such effects were seen. For purposes of this safety assessment, those scenarios are the post-application short-term dermal exposures and the short-term aggregate risk assessment. For the acute and chronic dietary assessments, EPA has determined that reliable data show the safety of infants and children would be adequately protected if the FQPA SF
were reduced to 1X. That decision is based on the following findings:
i. The toxicity database for fluindapyr is complete. Fluindapyr caused an increased in the thyroid follicular hypertrophy/hyperplasia in the 2generation reproduction study. The results of these findings raised concerns about the potential impact to the developing brain in response to changing thyroid levels brought on by thyroid effect in the parents. A database uncertainty factor of 10X is placed on fluindapyr to address this concern.
ii. In the acute neurotoxicity study ACN, decreases in total and ambulatory motor activities and in rearing were seen and could be considered as potential evidence for neurotoxicity. However, concern with fluindapyr is low because 1 no other effects were observed in database including in the subchronic neurotoxicity study SCN; 2 no neurohistopathology was found in the ACN, SCN or any toxicity study in the fluindapyr database; and 3 the toxicity endpoints and PoD selected for risk assessment are protective of the effects seen in the ACN.
iii. There is no evidence that fluindapyr results in increased quantitative or qualitative susceptibility in the developmental toxicity studies in rabbits or rats or the reproductive toxicity study in rats. In the 2generation reproduction study in rats, reproductive effects were observed, and offspring toxicity decreased pup weights in F1 and F2 generation;
thymus and spleen weights were decreased was observed in the presence same dosage of parental toxicity. Based on the effects in the 2-generation reproduction study, there is some uncertainty about the potential thyroidrelated effects on the developing fetus or child. While EPA is retaining the 10X
FQPA SF for short-term aggregate risk assessment, there is no concern for this uncertainty for the acute dietary exposure assessment because perturbation of thyroid after a single dose is not anticipated to impact the developing fetus or offspring. Nor is there a concern for this uncertainty in the chronic dietary assessment because the chronic dietary endpoint, based on
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