[Federal Register Volume 79, Number 63 (Wednesday, April 2, 2014)]
[Rules and Regulations]
[Pages 18461-18467]
From the Federal Register Online via the Government Publishing Office [www.gpo.gov]
[FR Doc No: 2014-07100]


-----------------------------------------------------------------------

ENVIRONMENTAL PROTECTION AGENCY

40 CFR Part 180

[EPA-HQ-OPP-2013-0051; FRL-9907-05]


Propiconazole; Pesticide Tolerances

AGENCY: Environmental Protection Agency (EPA).

ACTION: Final rule.

-----------------------------------------------------------------------

SUMMARY: This regulation establishes a tolerance for residues of 
propiconazole in or on the rapeseed crop subgroup 20A. Syngenta Crop 
Protection requested this tolerance under the Federal Food, Drug, and 
Cosmetic Act (FFDCA).

DATES: This regulation is effective April 2, 2014. Objections and 
requests for hearings must be received on or before June 2, 2014, and 
must be filed in accordance with the instructions provided in 40 CFR 
part 178 (see also Unit I.C. of the SUPPLEMENTARY INFORMATION).

ADDRESSES: The docket for this action, identified by docket 
identification (ID) number EPA-HQ-OPP-2013-0051, is available at http://www.regulations.gov or at the Office of Pesticide Programs Regulatory 
Public Docket (OPP Docket) in the Environmental Protection Agency 
Docket Center (EPA/DC), EPA West Bldg., Rm. 3334, 1301 Constitution 
Ave. NW., Washington, DC 20460-0001. The Public Reading Room is open 
from 8:30 a.m. to 4:30 p.m., Monday through Friday, excluding legal 
holidays. The telephone number for the Public Reading Room is (202) 
566-1744, and the telephone number for the OPP Docket is (703) 305-
5805. Please review the visitor instructions and additional information 
about the docket available at http://www.epa.gov/dockets.

FOR FURTHER INFORMATION CONTACT: Lois Rossi, Registration Division 
(7505P), Office of Pesticide Programs, Environmental Protection Agency, 
1200 Pennsylvania Ave. NW., Washington, DC 20460-0001; telephone 
number: (703) 305-7090; email address: [email protected].

SUPPLEMENTARY INFORMATION:

I. General Information

A. Does this action apply to me?

    You may be potentially affected by this action if you are an 
agricultural producer, food manufacturer, or pesticide manufacturer. 
The following list of North American Industrial Classification System 
(NAICS) codes is not intended to be exhaustive, but rather provides a 
guide to help readers

[[Page 18462]]

determine whether this document applies to them. Potentially affected 
entities may include:
     Crop production (NAICS code 111).
     Animal production (NAICS code 112).
     Food manufacturing (NAICS code 311).
     Pesticide manufacturing (NAICS code 32532).

B. How can I get electronic access to other related information?

    You may access a frequently updated electronic version of EPA's 
tolerance regulations at 40 CFR part 180 through the Government 
Printing Office's e-CFR site at http://www.ecfr.gov/cgi-bin/text-idx?&c=ecfr&tpl=/ecfrbrowse/Title40/40tab_02.tpl.

C. How can I file an objection or hearing request?

    Under FFDCA section 408(g), 21 U.S.C. 346a, any person may file an 
objection to any aspect of this regulation and may also request a 
hearing on those objections. You must file your objection or request a 
hearing on this regulation in accordance with the instructions provided 
in 40 CFR part 178. To ensure proper receipt by EPA, you must identify 
docket ID number EPA-HQ-OPP-2013-0051 in the subject line on the first 
page of your submission. All objections and requests for a hearing must 
be in writing, and must be received by the Hearing Clerk on or before 
June 2, 2014. Addresses for mail and hand delivery of objections and 
hearing requests are provided in 40 CFR 178.25(b).
    In addition to filing an objection or hearing request with the 
Hearing Clerk as described in 40 CFR part 178, please submit a copy of 
the filing (excluding any Confidential Business Information (CBI)) for 
inclusion in the public docket. Information not marked confidential 
pursuant to 40 CFR part 2 may be disclosed publicly by EPA without 
prior notice. Submit the non-CBI copy of your objection or hearing 
request, identified by docket ID number EPA-HQ-OPP-2013-0051, by one of 
the following methods:
     Federal eRulemaking Portal: http://www.regulations.gov. 
Follow the online instructions for submitting comments. Do not submit 
electronically any information you consider to be CBI or other 
information whose disclosure is restricted by statute.
     Mail: OPP Docket, Environmental Protection Agency Docket 
Center (EPA/DC), (28221T), 1200 Pennsylvania Ave. NW., Washington, DC 
20460-0001.
     Hand Delivery: To make special arrangements for hand 
delivery or delivery of boxed information, please follow the 
instructions at http://www.epa.gov/dockets/contacts.html.
    Additional instructions on commenting or visiting the docket, along 
with more information about dockets generally, is available at http://www.epa.gov/dockets.

II. Summary of Petitioned-for Tolerance

    In the Federal Register of February 15, 2013 (78 FR 11126) (FRL-
9378-4), EPA issued a document pursuant to FFDCA section 408(d)(3), 21 
U.S.C. 346a(d)(3), announcing the filing of a pesticide petition (PP 
2F8135) by Syngenta Crop Protection, LLC., P.O. Box 18300, Greensboro, 
NC 27419-8300. The petition requested that 40 CFR 180.434 be amended by 
establishing tolerances for residues of the fungicide propiconazole, 1-
[[2-(2,4-dichlorophenyl)-4-propyl-1,3-dioxolan-2-yl] methyl]-1H-1,2,4-
triazole, and its metabolites determined as 2,4,-dichlorobenzoic acid 
and expressed as parent compound, in or on rapeseed subgroup 20A at 0.3 
parts per million (ppm). That document referenced a summary of the 
petition prepared by Syngenta Crop Protection, the registrant, which is 
available in the docket, http://www.regulations.gov. Comments were 
received on the notice of filing. EPA's response to these comments is 
discussed in Unit IV.C.

III. Aggregate Risk Assessment and Determination of Safety

    Section 408(b)(2)(A)(i) of FFDCA allows EPA to establish a 
tolerance (the legal limit for a pesticide chemical residue in or on a 
food) only if EPA determines that the tolerance is ``safe.'' Section 
408(b)(2)(A)(ii) of FFDCA defines ``safe'' to mean that ``there is a 
reasonable certainty that no harm will result from aggregate exposure 
to the pesticide chemical residue, including all anticipated dietary 
exposures and all other exposures for which there is reliable 
information.'' This includes exposure through drinking water and in 
residential settings, but does not include occupational exposure. 
Section 408(b)(2)(C) of FFDCA requires EPA to give special 
consideration to exposure of infants and children to the pesticide 
chemical residue in establishing a tolerance and to ``ensure that there 
is a reasonable certainty that no harm will result to infants and 
children from aggregate exposure to the pesticide chemical residue. . . 
.''
    Consistent with FFDCA section 408(b)(2)(D), and the factors 
specified in FFDCA section 408(b)(2)(D), EPA has reviewed the available 
scientific data and other relevant information in support of this 
action. EPA has sufficient data to assess the hazards of and to make a 
determination on aggregate exposure for propiconazole including 
exposure resulting from the tolerances established by this action. 
EPA's assessment of exposures and risks associated with propiconazole 
follows.

A. Toxicological Profile

    EPA has evaluated the available toxicity data and considered its 
validity, completeness, and reliability as well as the relationship of 
the results of the studies to human risk. EPA has also considered 
available information concerning the variability of the sensitivities 
of major identifiable subgroups of consumers, including infants and 
children.
    The primary target organ for propiconazole toxicity in animals is 
the liver. Increased liver weights were seen in mice after subchronic 
or chronic oral exposures to propiconazole. Liver lesions such as 
vacuolation of hepatocytes, ballooned liver cells, foci of enlarged 
hepatocytes, hypertrophy and necrosis are characteristic of 
propiconazole toxicity in rats and mice. Decreased body weight gain was 
also seen in subchronic, chronic, developmental and reproductive 
studies in animal studies. Dogs appeared to be more sensitive to the 
localized toxicity of propiconazole as manifested by stomach 
irritations at 6 mg/kg/day and above.
    In rabbits, developmental toxicity occurred at a higher dose than 
the maternally toxic dose, while in rats, developmental toxicity 
occurred at lower doses than maternal toxic doses. Increased incidences 
of rudimentary ribs occurred in rat and rabbit fetuses. Increased cleft 
palate malformations were noted in two studies in rats. In one 
published study in rats, developmental effects (malformations of the 
lung and kidneys, incomplete ossification of the skull, caudal 
vertebrae and digits, extra rib (14th rib) and missing sternbrae) were 
reported at doses that were not maternally toxic. In the 2-generation 
reproduction study in rats, offspring toxicity occurred at a higher 
dose than the parental toxic dose suggesting lower susceptibility of 
the offspring to the toxic doses of propiconazole.
    The acute neurotoxicity study resulted in decreased motor activity 
at 300 mg/kg. The current acute dietary assessment is based on an 
endpoint more sensitive than the neurotoxicity in the acute 
neurotoxicity study. Based on a weight of evidence evaluation by the 
Agency, the subchronic neurotoxicity data requirement (SCN) was waived.

[[Page 18463]]

Propiconazole was negative for mutagenicity in the in vitro BALB/3T3 
cell transformation assay, bacterial reverse mutation assay, Chinese 
hamster bone marrow chromosomal aberration assay, unscheduled DNA 
synthesis studies in human fibroblasts and primary rat hepatocytes, 
mitotic gene conversion assay and the dominant lethal assay in mice. It 
caused proliferative changes in the rat liver with or without 
pretreatment with an initiator, like phenobarbital, a known liver tumor 
promoter. Liver enzyme induction studies with propiconazole in mice 
demonstrated that propiconazole is a strong phenobarbital type inducer 
of xenobiotic metabolizing enzymes. Hepatocellular proliferation 
studies in mice suggest that propiconazole induces cell proliferation 
followed by treatment-related hypertrophy in a manner similar to the 
known hypertrophic agent phenobarbital.
    Propiconazole was carcinogenic to male mice. Propiconazole was not 
carcinogenic to rats or to female mice. The Agency classified 
propiconazole as a possible human carcinogen and recommended that, for 
the purpose of risk characterization, the reference dose (RfD) approach 
be used for quantification of human risk. Propiconazole is not 
genotoxic and this fact, together with special mechanistic studies, 
indicates that propiconazole is a threshold carcinogen. Propiconazole 
produced liver tumors in male mice only at a high dose that was toxic 
to the liver. At doses below the RfD, liver toxicity is not expected; 
therefore, tumors are also not expected.
    Specific information on the studies received and the nature of the 
adverse effects caused by propiconazole as well as the no-observed-
adverse-effect-level (NOAEL) and the lowest-observed-adverse-effect-
level (LOAEL) from the toxicity studies can be found at http://www.regulations.gov in the document titled ``Propiconazole Human Health 
Risk Assessment for an Section 3 Registration on Rapeseed Crop Subgroup 
20A,'' pp. 41-47 in docket ID number EPA-HQ-OPP-2013-0051.

B. Toxicological Points of Departure/Levels of Concern

    Once a pesticide's toxicological profile is determined, EPA 
identifies toxicological points of departure (POD) and levels of 
concern to use in evaluating the risk posed by human exposure to the 
pesticide. For hazards that have a threshold below which there is no 
appreciable risk, the toxicological POD is used as the basis for 
derivation of reference values for risk assessment. PODs are developed 
based on a careful analysis of the doses in each toxicological study to 
determine the dose at which no adverse effects are observed (the NOAEL) 
and the lowest dose at which adverse effects of concern are identified 
(the LOAEL). Uncertainty/safety factors are used in conjunction with 
the POD to calculate a safe exposure level--generally referred to as a 
population-adjusted dose (PAD) or a reference dose (RfD)--and a safe 
margin of exposure (MOE). For non-threshold risks, the Agency assumes 
that any amount of exposure will lead to some degree of risk. Thus, the 
Agency estimates risk in terms of the probability of an occurrence of 
the adverse effect expected in a lifetime. For more information on the 
general principles EPA uses in risk characterization and a complete 
description of the risk assessment process, see http://www.epa.gov/pesticides/factsheets/riskassess.htm.
    A summary of the toxicological endpoints for propiconazole used for 
human risk assessment is discussed in Unit III.B. of the final rule 
published in the Federal Register of May 11, 2011 (76 FR 27261) (FRL-
8873-2).

C. Exposure Assessment

    1. Dietary exposure from food and feed uses. In evaluating dietary 
exposure to propiconazole, EPA considered exposure under the 
petitioned-for tolerances as well as all existing propiconazole 
tolerances in 40 CFR 180.434. EPA assessed dietary exposures from 
propiconazole in food as follows:
    i. Acute exposure. Quantitative acute dietary exposure and risk 
assessments are performed for a food-use pesticide, if a toxicological 
study has indicated the possibility of an effect of concern occurring 
as a result of a 1-day or single exposure. Such effects were identified 
for propiconazole. In estimating acute dietary exposure, EPA used food 
consumption information from the United States Department of 
Agriculture (USDA) National Health and Nutrition Examination Survey, 
What We Eat in America, (NHANES/WWEIA). This dietary survey was 
conducted from 2003 to 2008. As to residue levels in food, EPA 
conducted an acute dietary analysis for propiconazole residues of 
concern using tolerance levels and 100 percent crop treated (PCT) for 
all existing and proposed uses.
    ii. Chronic exposure. In conducting the chronic dietary exposure 
assessment EPA used the food consumption data from the USDA's NHANES/
WWEIA. This dietary survey was conducted from 2003 to 2008. As to 
residue levels in food, EPA conducted a chronic dietary analysis for 
propiconazole residues of concern using tolerance levels for some 
commodities, average field trial residues for the remaining 
commodities, and 100 PCT for all existing and proposed uses.
    iii. Cancer. EPA determines whether quantitative cancer exposure 
and risk assessments are appropriate for a food-use pesticide based on 
the weight of the evidence from cancer studies and other relevant data. 
Cancer risk is quantified using a linear or nonlinear approach. If 
sufficient information on the carcinogenic mode of action is available, 
a threshold or nonlinear approach is used and a cancer RfD is 
calculated based on an earlier noncancer key event. If carcinogenic 
mode of action data are not available, or if the mode of action data 
determines a mutagenic mode of action, a default linear cancer slope 
factor approach is utilized. Based on the data summarized in Unit 
III.A., EPA has concluded that a nonlinear RfD approach is appropriate 
for assessing cancer risk to propiconazole. Cancer risk was assessed 
using the same exposure estimates as discussed in Unit III.C.1.ii.
    iv. Anticipated residue information. Section 408(b)(2)(E) of FFDCA 
authorizes EPA to use available data and information on the anticipated 
residue levels of pesticide residues in food and the actual levels of 
pesticide residues that have been measured in food. If EPA relies on 
such information, EPA must require pursuant to FFDCA section 408(f)(1) 
that data be provided 5 years after the tolerance is established, 
modified, or left in effect, demonstrating that the levels in food are 
not above the levels anticipated. For the present action, EPA will 
issue such data call-ins as are required by FFDCA section 408(b)(2)(E) 
and authorized under FFDCA section 408(f)(1). Data will be required to 
be submitted no later than 5 years from the date of issuance of these 
tolerances.
    2. Dietary exposure from drinking water. The Agency used screening 
level water exposure models in the dietary exposure analysis and risk 
assessment for propiconazole in drinking water. These simulation models 
take into account data on the physical, chemical, and fate/transport 
characteristics of propiconazole. Further information regarding EPA 
drinking water models used in pesticide exposure assessment can be 
found at http://www.epa.gov/oppefed1/models/water/index.htm.
    Based on the Pesticide Root Zone Model/Exposure Analysis Modeling 
System (PRZM/EXAMS) and Screening Concentration in Ground Water (SCI-
GROW) models, the estimated drinking water concentrations (EDWCs) of

[[Page 18464]]

propiconazole for acute exposures are estimated to be 55.78 parts per 
billion (ppb) for surface water and 0.64 ppb for ground water, and for 
chronic exposures are estimated to be 21.61 ppb for surface water and 
0.64 ppb for ground water.
    Modeled estimates of drinking water concentrations were directly 
entered into the dietary exposure model. For acute dietary risk 
assessment, the water concentration value of 55.78 ppb was used to 
assess the contribution to drinking water. For chronic dietary risk 
assessment, the water concentration of value 21.61ppb was used to 
assess the contribution to drinking water.
    3. From 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).
    Propiconazole is currently registered for the following uses that 
could result in residential exposures: Turf, ornamentals, and in paint. 
The highest incidental oral and dermal exposure scenarios are expected 
from residential use on turf. EPA assessed short term risk to toddlers 
from incidental oral and dermal exposure and short-term risk to adults 
from dermal and inhalation residential handler exposure as well as from 
post-application dermal exposure. The highest post application exposure 
from residential use on turf was used to assess risk to short-term 
aggregate exposures.
    The only residential use scenario that will result in potential 
intermediate term exposure to propiconazole is dermal and incidental 
oral post application exposure to children from wood treatment. 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 408(b)(2)(D)(v) 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 pesticide's residues and ``other substances 
that have a common mechanism of toxicity.''
    Propiconazole is a member of the triazole-containing class of 
pesticides. Although conazoles act similarly in plants (fungi) by 
inhibiting ergosterol biosynthesis, there is not necessarily a 
relationship between their pesticidal activity and their mechanism of 
toxicity in mammals. Structural similarities do not constitute a common 
mechanism of toxicity. Evidence is needed to establish that the 
chemicals operate by the same, or essentially the same, sequence of 
major biochemical events (EPA, 2002). In conazoles, however, a variable 
pattern of toxicological responses is found; some are hepatotoxic and 
hepatocarcinogenic in mice. Some induce thyroid tumors in rats. Some 
induce developmental, reproductive, and neurological effects in 
rodents. Furthermore, the conazoles produce a diverse range of 
biochemical events including altered cholesterol levels, stress 
responses, and altered DNA methylation. It is not clearly understood 
whether these biochemical events are directly connected to their 
toxicological outcomes.
    Thus, there is currently no evidence to indicate that conazoles 
share common mechanisms of toxicity and EPA is not following a 
cumulative risk approach based on a common mechanism of toxicity for 
the conazoles. For information regarding EPA's procedures for 
cumulating effects from substances found to have a common mechanism of 
toxicity, see EPA's Web site at http://www.epa.gov/pesticides/cumulative.
    Propiconazole is a triazole-derived pesticide. This class of 
compounds can form the common metabolite 1,2,4-triazole and two 
triazole conjugates (triazolylalanine and triazolylacetic acid). To 
support existing tolerances and to establish new tolerances for 
triazole-derivative pesticides, including propiconazole, U.S. EPA 
conducted a human health risk assessment for exposure to 1,2,4-
triazole, triazolylalanine, and triazolylacetic acid resulting from the 
use of all current and pending uses of any triazole-derived fungicide. 
The risk assessment is a highly conservative, screening-level 
evaluation in terms of hazards associated with common metabolites 
(e.g., use of a maximum combination of uncertainty factors) and 
potential dietary and non-dietary exposures (i.e., high end estimates 
of both dietary and non-dietary exposures). In addition, the Agency 
retained the additional 10X FQPA safety factor for the protection of 
infants and children. The assessment includes evaluations of risks for 
various subgroups, including those comprised of infants and children. 
The Agency's complete risk assessment is found in the propiconazole 
reregistration docket at http://www.regulations.gov, Docket 
Identification (ID) Number EPA-HQ-OPP-2005-0497.
    An updated dietary exposure and risk analysis for the common 
triazole metabolites 1,2,4-triazole (T), triazolylalanine (TA), 
triazolylacetic acid (TAA), and triazolylpyruvic acid (TP) was 
completed on October 24, 2013, in association with registration 
requests for several triazole fungicides (propiconazole, 
difenoconazole, and tebuconazole). That analysis concluded that risk 
estimates were below the Agency's level of concern for all population 
groups. This assessment may be found on http://www.regulations.gov by 
searching for the following title and docket number: ``Common Triazole 
Metabolites: Updated Aggregate Human Health Risk Assessment to Address 
The New Section 3 Registrations For Use of Propiconazole on Rapeseed 
Crop Subgroup 20A; Use of Difenoconazole on Rapeseed Crop Subgroup 20A; 
and Use of Tebuconazole on Imported Oranges'' (located in docket ID 
number EPA-HQ-OPP-2013-0051).

D. Safety Factor for Infants and Children

    1. In general. Section 408(b)(2)(C) 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 study in rats, fetal effects observed in this study at a dose 
lower than that evoking maternal toxicity are considered to be 
quantitative evidence of increased susceptibility of fetuses to in 
utero exposure to propiconazole. In the developmental toxicity study in 
rabbits, neither quantitative nor qualitative evidence of increased 
susceptibility of fetuses to in utero exposure to propiconazole was 
observed in this study. In the 2-generation reproduction study in rats, 
neither quantitative nor qualitative evidence of increased 
susceptibility of neonates (as compared to adults) to prenatal and/or 
postnatal exposure to propiconazole was observed. There is no evidence 
of neuropathology or abnormalities in the development of the fetal 
nervous system from the available toxicity studies conducted with 
propiconazole. In the rat acute neurotoxicity study, there was evidence 
of mild neurobehavioral

[[Page 18465]]

effects at 300 mg/kg, but no evidence of neuropathology from 
propiconazole administration. Although there was quantitative evidence 
of increased susceptibility of the young following exposure to 
propiconazole in the developmental rat study, the Agency determined 
there is a low degree of concern for this finding and no residual 
uncertainties because the increased susceptibility was based on minimal 
toxicity at high doses of administration, clear NOAELs and LOAELs have 
been identified for all effects of concern, and a clear dose-response 
has been well defined.
    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 propiconazole is complete. The most 
recently published Federal Register notice on April 19, 2013 (78 FR 
23497) (FRL-9381-8) cited an immunotoxicity study as a data gap, but 
since the publication of that final rule, the Agency has evaluated and 
granted a waiver request for this data requirement for the conazoles as 
a class based on the following considerations:
     There was no evidence of adverse effects on the immune 
system in mice, rats, or dogs in the data base for any of the conazole 
pesticides.
     The liver, not the immune system, is generally the target 
organ for this chemical class, and hepatotoxicity or body weight 
changes are the primary toxicological endpoints of concern and were 
used in risk assessments.
     The conazoles do not belong to a class of chemicals (e.g., 
the organotins, heavy metals, or halogenated aromatic hydrocarbons) 
that would be expected to be immunotoxic.
    There was no evidence of immunotoxicity with six other 
structurally-related conazole fungicides, namely, flutriafol, 
metconazole, tebuconazole, tetraconazole, triadimefon, and 
triticonazole. For another conazole fungicide, triflumizole, the 
effects on the immune system occurred only at the highest dose tested. 
Immunotoxicity was demonstrated with difenoconazole, however it was 
observed in the presence of systemic toxicity and at a relatively high 
dose. PODs based on the most sensitive endpoints obtained via the 
appropriate routes of exposure in the most sensitive species are 
currently used for dietary and non-dietary risk assessments.
    All these factors indicate that an immunotoxicity study would most 
likely not result in an adverse effect that could be used as an 
endpoint for conazole risk assessment. Based on a weight of evidence 
approach, the Agency concluded that immunotoxicity studies are not 
required for propiconazole. An immunotoxicity study is not anticipated 
to provide a lower POD or result in a more sensitive endpoint than 
those already used. Based on a weight of the evidence approach, EPA has 
waived the requirement for a subchronic neurotoxicity study for 
propiconazole. This data waiver was based on the following 
considerations:
    i. Other than the mild effects seen at 300 mg/kg in the acute 
neurotoxicity study, the lack of neurotoxicity and neurobehavioral 
effects seen in the propiconazole toxicity database;
    ii. The liver, not the nervous system, is the primary target organ 
of propiconazole toxicity, and decreased body weight is the most 
sensitive endpoint in repeated-dose studies. EPA concludes that a 
subchronic neurotoxicity study is unlikely to provide a lower endpoint 
than those currently used for risk assessment.
    Finally, EPA waived the requirement for a subchronic inhalation 
data based on, among other things, its conclusion that even if an 
additional 10X safety factor was applied, inhalation exposure would not 
raise a risk of concern.
    iii. Although an apparent increased quantitative susceptibility was 
observed in fetuses and offspring, for the reasons noted in this unit 
residual uncertainties or concerns for prenatal and/or postnatal 
toxicity are minimal.
    iv. There are no residual uncertainties identified in the exposure 
databases. The acute dietary food exposure assessments were performed 
based on 100 PCT and tolerance-level residues, while the chronic used a 
combination of tolerance-level residues and reliable data on average 
field trial residues and 100 PCT. EPA made conservative (protective) 
assumptions in the ground and surface water modeling used to assess 
exposure to propiconazole in drinking water. EPA used similarly 
conservative assumptions to assess post-application exposure of 
children as well as incidental oral exposure of toddlers. These 
assessments will not underestimate the exposure and risks posed by 
propiconazole.

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. Using the exposure assumptions discussed in this 
unit for acute exposure, the acute dietary exposure from food and water 
to propiconaozle will occupy 84% of the aPAD for children 1-2 years 
old, the population group receiving the greatest exposure.
    2. Chronic risk. Using the exposure assumptions described in this 
unit for chronic exposure, EPA has concluded that chronic exposure to 
propiconazole from food and water will utilize 24% of the cPAD for 
children 1-2 years old, the population group receiving the greatest 
exposure. Based on the explanation in Unit III.C.3., regarding 
residential use patterns, chronic residential exposure to residues of 
propiconazole is not expected.
    3. Short-term risk. Short-term aggregate exposure takes into 
account short-term residential exposure plus chronic exposure to food 
and water (considered to be a background exposure level). Propiconazole 
is currently registered for uses that could result in short-term 
residential exposure, and the Agency has determined that it is 
appropriate to aggregate chronic exposure through food and water with 
short-term residential exposures to propiconazole.
    Using the exposure assumptions described in this unit for short-
term exposures, EPA has concluded the combined short-term food, water, 
and residential exposures result in aggregate MOEs from post-
application activities (the highest exposure scenario) of 200 for 
adults and 96 for children 1-2 years old. This assessment is considered 
conservative since it is based on a combination of tolerance-level 
residues and reliable data on average field trial residues and 100 PCT, 
conservative assumptions in the ground and surface water modeling, and 
conservative assumptions to assess post-application exposure of 
children as well as incidental oral exposure of toddlers. Additionally, 
the assessment could be further refined by using PCT estimates and 
anticipated residues for all crops. Accordingly, even though this MOE 
for children 1-2 years old is slightly below the target MOE of 100, the 
difference is small and is more than offset by the conservative 
exposure assumptions and therefore not of concern.

[[Page 18466]]

    4. Intermediate-term risk. Intermediate-term aggregate exposure 
takes into account intermediate-term residential exposure plus chronic 
exposure to food and water (considered to be a background exposure 
level).
    Propiconazole is currently registered for use as a wood treatment 
that could result in intermediate-term residential exposure, and the 
Agency has determined that it is appropriate to aggregate chronic 
exposure through food and water with intermediate-term residential 
exposures to propiconazole.
    Using the exposure assumptions described in this unit for 
intermediate-term exposures, EPA has concluded that the combined 
intermediate-term food, water, and residential exposures result in an 
aggregate MOE of 110 for children 1-2 years old. Because EPA's level of 
concern for propiconazole is a MOE of 100 or below, this MOE is not of 
concern.
    5. Aggregate cancer risk for U.S. population. EPA considers the 
chronic aggregate risk assessment to be protective of any aggregate 
cancer risk.
    6. Determination of safety. Based on these risk assessments, EPA 
concludes that there is a reasonable certainty that no harm will result 
to the general population or to infants and children from aggregate 
exposure to propiconazole residues.

IV. Other Considerations

A. Analytical Enforcement Methodology

    Adequate enforcement methodology, a high performance liquid 
chromatography with ultraviolet detection method (HPLC/UV Method AG-
671A) is available to enforce the tolerance expression. The method may 
be requested from: Chief, Analytical Chemistry Branch, Environmental 
Science Center, 701 Mapes Rd., Ft. Meade, MD 20755-5350; telephone 
number: (410) 305-2905; email address: [email protected].

B. International Residue Limits

    In making its tolerance decisions, EPA seeks to harmonize U.S. 
tolerances with international standards whenever possible, consistent 
with U.S. food safety standards and agricultural practices. EPA 
considers the international maximum residue limits (MRLs) established 
by the Codex Alimentarius Commission (Codex), as required by FFDCA 
section 408(b)(4). The Codex Alimentarius is a joint United Nations 
Food and Agriculture Organization/World Health Organization food 
standards program, and it is recognized as an international food safety 
standards-setting organization in trade agreements to which the United 
States is a party. EPA may establish a tolerance that is different from 
a Codex MRL; however, FFDCA section 408(b)(4) requires that EPA explain 
the reasons for departing from the Codex level.
    The Codex has established MRLs for propiconazole in or on rapeseed 
at 0.02 ppm. This MRL is different than the tolerance being established 
for propiconazole in the United States, which, as noted earlier, is 0.3 
ppm. The approved uses for propiconazole in the United States will 
result in residues that exceed the Codex MRLs.

C. Response to Comments

    The Agency received a comment objecting to the presence of any 
pesticide residues on crops and stated that EPA should set no pesticide 
tolerance greater than zero. The comment also stated that the Agency 
should have more information on long term testing before moving 
forward. A second comment also objected to this petition and stated 
that this product should be banned and never used and never produced in 
the USA. In addition, the second comment also noted several adverse 
effects seen in animal toxicology studies with propiconazole and claims 
because of these effects no tolerance should be approved. The Agency 
understands the concerns raised in the comments and recognizes that 
some individuals believe that pesticides should be banned completely. 
However, the existing legal framework provided by section 408 of the 
Federal Food, Drug and Cosmetic Act (FFDCA), contemplates that 
tolerances greater than zero may be set when persons seeking such 
tolerances or exemptions have demonstrated that the pesticide meets the 
safety standard imposed by that statute. The comments appear to be 
directed at the underlying statute and not EPA's implementation of it; 
no contention has been made that EPA has acted in violation of the 
statutory framework. In addition, EPA has found that there is a 
reasonable certainty of no harm to humans after considering these 
toxicological studies and the exposure levels of humans to 
propiconazole.
    A third comment dealt with a different chemical entirely and thus 
needs no response.

V. Conclusion

    Therefore, a tolerance is established for residues of 
propiconazole, 1-[[2-(2,4-dichlorophenyl)-4-propyl-1,3-dioxolan-2-
yl]methyl]-1H-1,2,4-triazole, and its metabolites determined as 2,4,-
dichlorobenzoic acid and expressed as parent compound, in or on 
rapeseed subgroup 20A at 0.30 ppm.

VI. Statutory and Executive Order Reviews

    This final rule establishes tolerances under FFDCA section 408(d) 
in response to a petition submitted to the Agency. The Office of 
Management and Budget (OMB) has exempted these types of actions from 
review under Executive Order 12866, entitled ``Regulatory Planning and 
Review'' (58 FR 51735, October 4, 1993). Because this final rule has 
been exempted from review under Executive Order 12866, this final rule 
is not subject to Executive Order 13211, entitled ``Actions Concerning 
Regulations That Significantly Affect Energy Supply, Distribution, or 
Use'' (66 FR 28355, May 22, 2001) or Executive Order 13045, entitled 
``Protection of Children from Environmental Health Risks and Safety 
Risks'' (62 FR 19885, April 23, 1997). This final rule does not contain 
any information collections subject to OMB approval under the Paperwork 
Reduction Act (PRA) (44 U.S.C. 3501 et seq.), nor does it require any 
special considerations under Executive Order 12898, entitled ``Federal 
Actions to Address Environmental Justice in Minority Populations and 
Low-Income Populations'' (59 FR 7629, February 16, 1994).
    Since tolerances and exemptions that are established on the basis 
of a petition under FFDCA section 408(d), such as the tolerance in this 
final rule, do not require the issuance of a proposed rule, the 
requirements of the Regulatory Flexibility Act (RFA) (5 U.S.C. 601 et 
seq.), do not apply.
    This final rule directly regulates growers, food processors, food 
handlers, and food retailers, not States or tribes, nor does this 
action alter the relationships or distribution of power and 
responsibilities established by Congress in the preemption provisions 
of FFDCA section 408(n)(4). As such, the Agency has determined that 
this action will not have a substantial direct effect on States or 
tribal governments, on the relationship between the national government 
and the States or tribal governments, or on the distribution of power 
and responsibilities among the various levels of government or between 
the Federal Government and Indian tribes. Thus, the Agency has 
determined that Executive Order 13132, entitled ``Federalism'' (64 FR 
43255, August 10, 1999) and Executive Order 13175, entitled 
``Consultation and Coordination with Indian Tribal Governments'' (65 FR 
67249, November 9, 2000) do not apply to this final rule. In addition, 
this final

[[Page 18467]]

rule does not impose any enforceable duty or contain any unfunded 
mandate as described under Title II of the Unfunded Mandates Reform Act 
of 1995 (UMRA) (2 U.S.C. 1501 et seq.).
    This action does not involve any technical standards that would 
require Agency consideration of voluntary consensus standards pursuant 
to section 12(d) of the National Technology Transfer and Advancement 
Act of 1995 (NTTAA) (15 U.S.C. 272 note).

VII. Congressional Review Act

    Pursuant to the Congressional Review Act (5 U.S.C. 801 et seq.), 
EPA will submit a report containing this rule and other required 
information to the U.S. Senate, the U.S. House of Representatives, and 
the Comptroller General of the United States prior to publication of 
the rule in the Federal Register. This action is not a ``major rule'' 
as defined by 5 U.S.C. 804(2).

List of Subjects in 40 CFR Part 180

    Environmental protection, Administrative practice and procedure, 
Agricultural commodities, Pesticides and pests, Reporting and 
recordkeeping requirements.

    Dated: March 21, 2014.
Lois Rossi,
Director, Registration Division, Office of Pesticide Programs.

    Therefore, 40 CFR chapter I is amended as follows:

PART 180--[AMENDED]

0
1. The authority citation for part 180 continues to read as follows:

    Authority:  21 U.S.C. 321(q), 346a and 371.


0
2. In Sec.  180.434, add alphabetically the following commodity to the 
table in paragraph (a) to read as follows:


Sec.  180.434  Propiconazole; tolerances for residues.

    (a) * * *

------------------------------------------------------------------------
                                                              Parts per
                         Commodity                             million
------------------------------------------------------------------------
 
                                * * * * *
Rapeseed subgroup 20A......................................         0.30
 
                                * * * * *
------------------------------------------------------------------------

* * * * *
[FR Doc. 2014-07100 Filed 4-1-14; 8:45 am]
BILLING CODE 6560-50-P