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Federal Register / Vol. 86, No. 179 / Monday, September 20, 2021 / Rules and Regulations
consumption surveys, EPA does not have available reliable information on the regional consumption of food to which pyraclostrobin may be applied in a particular area.
2. Dietary exposure from drinking water. The Agency used screening level water exposure models in the dietary exposure analysis and risk assessment for pyraclostrobin in drinking water.
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.
Based on the Pesticide in Water Calculator PWC, for the acute dietary risk assessment, EPA used an estimated drinking water concentration EDWC of 22 ppb into the DEEMFCID Model. For the chronic exposure assessment, EPA
used a value of 0.99 ppb.
3. Non-dietary exposure. The term residential exposure is used in this document to refer to non-occupational, non-dietary exposure e.g., for lawn and garden pest control, indoor pest control, termiticides, and flea and tick control on pets.
Pyraclostrobin is currently registered for uses that may result in residential handler and post-application exposures, including commercial and residential use on lawns, as well as commercial use on ornamental turf and trees, golf courses, and parks.
Based upon the hazard analysis for pyraclostrobin, short-term residential exposure that is available to be aggregated include incidental oral exposure e.g., hand-to-mouth or objectto-mouth. Hand-to-mouth and objectto-mouth scenarios are considered interrelated, and it is likely that they occur interspersed amongst each other across time; combining these scenarios would be overly conservative. Residential short and intermediate-term dermal exposures from children, youth, or adult scenarios are not being combined with incidental oral exposure due to differing endpoints selected. Based upon the available scenarios, incidental oral hand-to-mouth exposures were used in the pyraclostrobin short-term aggregate assessment.
Further information regarding EPA
standard assumptions and generic inputs for residential exposures may be found at http www2.epa.gov/pesticidescience-and-assessing-pesticide-risks/
standard-operating-proceduresresidential-pesticide.
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
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tolerance, the Agency consider available information concerning the cumulative effects of a particular pesticides residues and other 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 pyraclostrobin and any other substances and pyraclostrobin does not appear to produce a toxic metabolite produced by other substances. For the purposes of this tolerance action, therefore, EPA has not assumed that pyraclostrobin 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 rat developmental toxicity study, skeletal variations occurred at doses greater than or equal to those doses causing maternal toxicity i.e., diarrhea, decreased body weight, food consumption, and clinical signs of toxicity. In the rabbit developmental study, increased resorptions per litter, increased post-implantation loss, and dams with total resorptions were observed. Since the cause of fetal death is undetermined and may be attributed to either maternal or direct embryo fetal toxicity, the effect is part of both the maternal and developmental LOAEL. In one rat reproduction study, systemic toxicity manifested as decreased body weights in both the parents and offspring, with offspring effects occurring at a higher dose level than parental toxicity. In the second rat reproduction study, no toxicity was observed in both parents and offspring.
Therefore, there was no evidence of increased susceptibility quantitatively following pre-natal exposure to rats and rabbits in the developmental studies nor following preand post-natal exposure
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to rats in the multi-generation reproduction studies.
3. Conclusion. 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 pyraclostrobin is complete.
ii. There are no indications in any of the studies available that the nervous system is a target for pyraclostrobin. In the absence of definitive neurotoxicity or neuropathology findings in the neurotoxicity battery or elsewhere in the database, a developmental neurotoxicity study is not required.
iii. For the reasons summarized in section III.D.2, the degree of concern for prenatal and postnatal toxicity is low.
iv. There are no residual uncertainties identified in the exposure databases. The acute dietary exposure assessments were performed assuming 100 percent of the crops were treated with pyraclostrobin and incorporating tolerance-level or highest field trial residues. The chronic dietary exposure assessments were performed using average PCT estimates and tolerance-level or average field trial residues for crops in the screening level use analysis SLUA, while 100 PCT
was used for crops not included in the SLUA.
EPA made conservative protective assumptions in the ground and surface water modeling used to assess exposure to pyraclostrobin in drinking water. Although the acute and chronic assessments included minor refinements, the use of field trial and PCT estimates ensures that actual exposures/
risks from residues in food will not be underestimated. Although some of the residue values used in the dietary exposure assessment were refined, these assessments will not underestimate the dietary exposure to pyraclostrobin.

E. Aggregate Risks and Determination of Safety EPA determines whether acute and chronic dietary pesticide exposures are safe by comparing aggregate exposure estimates to the acute PAD aPAD and chronic PAD cPAD. For linear cancer risks, EPA calculates the lifetime probability of acquiring cancer given the estimated aggregate exposure. Short-, intermediate-, and chronic-term risks are evaluated by comparing the estimated aggregate food, water, and residential exposure to the appropriate PODs to ensure that an adequate MOE
exists.
1. Acute risk. An acute aggregate risk assessment takes into account acute exposure estimates from dietary consumption of food and drinking water. Using the exposure assumptions described in this unit for acute exposure, EPA has concluded that acute exposure to pyraclostrobin from food and water will utilize 86% of the aPAD
for females 13 to 49 years old, the only
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