美国制定萘乙酸酯残留限量要求（Naphthalene Acetates; Pesticide Tolerances)_中国食品网

【发布单位】 EPA
【发布文号】
【发布日期】 2015/12/14
【生效日期】 2015/12/14
【废止日期】
【替代法规】
【效　　力】
【食品伙伴网解读】 2015年12月14日美国环保署发布一则最终条例，修订萘乙酸酯在石榴中的残留限量要求。美国区际研究项目4号请求按照联邦食品、药品与化妆品法案的要求，对有关限量进行审查。经评估后，美国环保署将石榴中萘乙酸酯的最大限量分别定为0.05ppm。本条例自发布之日起生效，按40CFR§178的说明在2016年2月12日前提交反对或听证要求。

ACTION

Final Rule.

SUMMARY

This regulation establishes a tolerance for residues of the naphthalene acetate group in or on pomegranate. Interregio nal Research Project Number 4 (IR-4) requested the tolerance under the Federal Food, Drug, and Cosmetic Act (FFDCA).

TABLE OF CONTENTS

DATES:

ADDRESSES:

FOR FURTHER INFORMATION CONTACT:

SUPPLEMENTARY INFORMATION:

I. General Information

A. Does this action apply to me?

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

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

II. Summary of Petitioned-For Tolerance

III. Aggregate Risk Assessment and Determination of Safety

A. Toxicological Profile

B. Toxicological Points of Departure/Levels of Concern

C. Exposure Assessment

D. Safety Factor for Infants and Children

E. Aggregate Risks and Determination of Safety

IV. Other Considerations

A. Analytical Enforcement Methodology

B. Internatio nal Residue Limits

V. Conclusion

VI. Statutory and Executive Order Reviews

VII. Co ngressional Review Act

List of Subjects in 40 CFR Part 180

PART 180—[AMENDED]

TABLES

Table 1—Summary of Toxicological Doses and Endpoints for NAA for Use in Human Health Risk Assessment

DATES:

This regulation is effective December 14, 2015. Objections and requests for hearings must be received on or before February 12, 2016, 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-2014-0769, is available at http://www.regulations.gov or at the Office of Pesticide Programs Regulatory Public Docket (OPP Docket) in the Enviro nmental Protection Agency Docket Center (EPA/DC), West William Jefferson Clinton Bldg., Rm. 3334, 1301 Co nstitution Ave. NW., Washington, DC 20460-0001. The Public Reading Room is open from 8:30 a.m. to 4:30 p.m., Mo nday 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 additio nal information a bout the docket available at http://www.epa.gov/dockets.

FOR FURTHER INFORMATION CONTACT:

Susan Lewis, Registration Division (7505P), Office of Pesticide Programs, Enviro nmental Protection Agency, 1200 Pennsylvania Ave. NW., Washington, DC 20460-0001; main telephone number: (703) 305-7090; email address: RDFRNotices@epa.gov.

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 determine whether this docu ment 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 electro nic access to other related information?

You may access a frequently updat ed electro nic 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-2014-0769 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 February 12, 2016. 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 Co nfidential Business Information (CBI)) for inclusion in the public docket. Information not marked co nfidential 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-2014-0769, by one of the following methods:

Federal eRulemaking Portal: http://www.regulations.gov. Follow the o nline instructions for submitting comments. Do not submit electro nically any information you co nsider to be CBI or other information whose disclosure is restricted by statute.

Mail: OPP Docket, Enviro nmental 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.

Additio nal instructions on commenting or visiting the docket, along with more information a bout dockets generally, is available at http://www.epa.gov/dockets.

II. Summary of Petitioned-For Tolerance

In the Federal Register of February 11, 2015 (80 FR 7559) (FRL-9921-94), EPA issued a docu ment pursuant to FFDCA section 408(d)(3), 21 U.S.C. 346a(d)(3), announcing the filing of a pesticide petition (PP 4E8310) by IR-4, IR-4 Project Headquarters, 500 College Road East, Suite 201 W, Princeton, NJ. The petition requested that 40 CFR 180.155 be amended by establishing tolerances for residues of a family of plant growth regulators, the naphthalene acetates, in or on pomegranate at 0.05 parts per million (ppm). That docu ment referenced a summary of the petition prepared by AMVAC Chemical Corporation, the registrant, which is available in the docket, http://www.regulations.gov. There were no comments received in respo nse to the notice of filing.

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) o nly if EPA determines that the tolerance is “safe.” Section 408(b)(2)(A)(ii) of FFDCA defines “safe” to mean that “there is a reaso nable 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 occupatio nal exposure. Section 408(b)(2)(C) of FFDCA requires EPA to give special co nsideration to exposure of infants and children to the pesticide chemical residue in establishing a tolerance and to “ensure that there is a reaso nable certainty that no harm will result to infants and children from aggregate exposure to the pesticide chemical residue. . . .”

Co nsistent 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 the naphthalene acetates including exposure resulting from the tolerances established by this action. EPA's assessment of exposures and risks associated with the naphthalene acetates follows.

A. Toxicological Profile

EPA has e valuated the available toxicity data and co nsidered their validity, completeness, and reliability as well as the relatio nship of the results of the studies to human risk. EPA has also co nsidered available information co ncerning the variability of the sensitivities of major identifiable subgroups of consumers, including infants and children.

In this regulatory action, 1-naphthaleneacetic acid is a species of chemical that includes several similar compounds: Naphthaleneacetamide (NAA acetamide), naphthaleneacetic acid, potassium naphthaleneacetate (NAA potassium salt), ammo nium naphthaleneacetate (ammo nium NAA), sodium naphthaleneacetate (NAA sodium salt), and ethyl naphthaleneacetate (NAA ethyl ester). These chemicals are assessed as a single group and are collectively referred to as the naphthalene acetates (NAA). Hereafter, NAA will be used to refer to the entire naphthalene acetate group. These chemical compounds are structurally related, me tabolized to the acid form (by both plants and animals), and are eliminated from the body as glycine and glucuro nic acid co njugates within 36 to 48 hours after exposure. EPA has co ncluded that toxicity testing on any of these compounds should serve for all members of this group of chemicals.

In general, NAA sodium salt was the most toxic form in sub-chro nic and chro nic studies. Repeated exposure in oral toxicity studies resulted in decreased body weights and body weight gains accompanied by decreased food consumption. The major target organs of sub-chro nic and chro nic oral exposure were the liver, stomach, and lung. Others symptoms of toxicity from oral exposure included decreased hematocrit and hemoglobin, reduced red blood cell (RBC) count in rats and dogs, and hypocellularity of the bone marrow in dogs. In co ntrast to oral exposures, NAA ethyl ester was the most toxic chemical species when administered dermally, inducing epidermal hyperplasia and hyperkeratosis, sebaceous gland hyperplasia, and dermal inflammation. The NAA sodium salt required a 10-fold higher dose to elicit similar dermal effects and no dermal effects were noted in the NAA acetamide exposure. Systemic toxicity was not a co nsequence of dermal exposure to any of the tested naphthalene acetates.

Developmental and offspring toxicity was l inked to NAA sodium salt exposure but was not a common observation for the entire naphthalene acetate group. Developing rats exhibited decreased fetal weight and minor skeletal changes and were more susceptible to NAA sodium salt toxicity than the maternal rats. Skeletal defects and variants were observed in rabbit fetuses after exposure to NAA sodium salt in the developmental rabbit study; however these effects o nly occurred at doses that also compromised maternal health. Offspring toxicity from NAA sodium salt manifested as reduced litter survival and pup weight throughout lactation in two generations. These effects coincided with reduced body weight in both parental generations indicating the adults and their young were equally susceptible to NAA sodium salt.

Carcinogenicity studies of NAA acetamide in mice and NAA sodium salt in rats and mice are co nsidered adequate for the e valuation of the o ncogenicity of the NAA group. In these three studies the tested NAA compounds were not carcinogenic in mice or rats.

Specific information on the studies received and the nature of the adverse effects caused by NAA 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 docu ment, “Naphthalene Acetate. Human Health Risk Assessment for a Proposed New Use on Pomegranate” at pp. 31 in docket ID number EPA-HQ-OPP-2014-0769.

B. Toxicological Points of Departure/Levels of Concern

o nce a pesticide's toxicological profile is determined, EPA identifies toxicological points of departure (POD) and levels of co ncern to use in e valuating 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 ba sed on a careful analysis of the doses in each toxicological study to determine the dose at which the NOAEL and the LOAEL are identified. Uncertainty/safety factors are used in co njunction 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 des cription of the risk assessment process, see http://www2.epa.gov/pesticide-science-and-assessing-pesticide-risks/assessing-human-health-risk-pesticides.

A summary of the toxicological endpoints for NAA used for human risk assessment is shown in Table 1 of this unit.

Table 1—Summary of Toxicological Doses and Endpoints for NAA for Use in Human Health Risk Assessment Back to Top

Exposure/scenarioPoint of departure and uncertainty/safety factorsRfD, PAD, LOC for risk assessmentStudy and toxicological effects

LOC = level of concern. Point of Departure (POD) = A data point or an estimated point that is derived from observed dose-respo nse data and used to mark the beginning of extrapolation to determine risk associated with lower enviro nmentally relevant human exposures. Mg/kg/day = milligram/kilogram/day. NOAEL = no observed adverse effect level. LOAEL = lowest observed adverse effect level. UF = uncertainty factor. UF A = extrapolation from animal to human (interspecies). UF H = potential variation in sensitivity among members of the human population (intraspecies). FQPA SF = Food Quality Protection Act Safety Factor. PAD = population adjusted dose (c = chronic). RfD = reference dose.

1?The NOAEL/LOAEL used to set endpoints for the co-critical dog studies are in bold.

2?Inhalation absorption is assumed to be equivalent to oral absorption.

3?FQPA SF for inhalation accounts for the lack of an inhalation study.

Acute dietary (General population including infants and children)An acute RfD for the general population or any population subgroups was not selec ted because no effect attributable to a single exposure was observed in animal studies.

Chro nic dietary (All populations)NOAEL = 25 mg/kg/day UF A = 10x UF H = 10x FQPA SF = 1xChro nic RfD = 0.25 mg/kg/day cPAD = 0.25 mg/kg/dayCo-critical Dog Studies with NAA Na salt: Subchro nic Toxicity. Chro nic Toxicity. Subchronic.1 LOAEL = 150 mg/kg/day ba sed on GI tract lesions and hypocellularity of the bone marrow. Subchro nic NOAEL = 25 mg/kg/day.

?Chro nic LOAEL = 75 mg/kg/day ba sed on stomach lesions in 75% of the males and slight sinusoidal histiocytosis in the liver of 50% of the males.

Adult Oral Short-term (1-30 Days)NOAEL = 25 mg/kg/day UF A = 10x UF H = 10x FQPA SF = 1xLOC = 100Co-critical Dog Studies with NAA Na salt: Subchro nic Toxicity. Chro nic Toxicity. Subchro nic LOAEL = 150 mg/kg/day ba sed on GI tract lesions and hypocellularity of the bone marrow. Subchro nic NOAEL = 25 mg/kg/day.

?Chro nic LOAEL = 75 mg/kg/day ba sed on stomach lesions in 75% of the males and slight sinusoidal histiocytosis in the liver of 50% of the males.

?Chro nic NOAEL = 15 mg/kg/day.

Inhalation Short-Term (1-30 days)NOAEL = 25 mg/kg/day?2 UF A = 10x UF H = 10x FQPA SF = 10x?3LOC = 1000Co-critical Dog Studies with NAA Na salt: Subchro nic Toxicity. Chro nic Toxicity. Subchro nic LOAEL = 150 mg/kg/day ba sed on GI tract lesions and hypocellularity of the bone marrow.

?Subchro nic NOAEL = 25 mg/kg/day.

?Chro nic LOAEL = 75 mg/kg/day ba sed on stomach lesions in 75% of the males and slight sinusoidal histiocytosis in the liver of 50% of the males.

?Chro nic NOAEL = 15 mg/kg/day.

CancerNot carcinogenic ba sed on rats and mice bioassays. Not mutagenic.

C. Exposure Assessment

1. Dietary exposure from food and feed uses. In e valuating dietary exposure to NAA, EPA co nsidered exposure under the petitioned-for tolerance as well as all existing NAA tolerances in 40 CFR 180.155. EPA assessed dietary exposure to NAA 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 co ncern occurring as a result of a 1-day or single exposure. No such effects were identified in the toxicological studies for NAA; therefore, a quantitative acute dietary exposure assessment is unnecessary.

ii. Chro nic exposure. In co nducting the chro nic dietary exposure assessment EPA used the Dietary Exposure e valuation Model software with the Food Commodity Intake Databa se (DEEM-FCID), Version 3.16, which incorporates 2003-2008 food co nsumption data from the U.S. Department of Agriculture's (USDA's) Natio nal Health and Nutrition Examination Survey, What We Eat in America, (NHANES/WWEIA). DEEM default processing factors were used to modify the tolerance values. As to NAA residues levels in food, tolerance-level residues and 100 percent crop treated (PCT) assumptions were applied for all affected crops.

iii. Cancer. ba sed on the data summarized in Unit III.A., EPA has co ncluded that NAA does not pose a cancer risk to humans. Therefore, a dietary exposure assessment for the purpose of assessing cancer risk is unnecessary.

iv. Anticipated residue and percent crop treated (PCT) information. EPA did not use anticipated residue and/or PCT information in the dietary assessment for NAA. Tolerance level residues and 100 PCT were 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 NAA in drinking water. These simulation models take into account data on the physical, chemical, and fate/transport characteristics of NAA. Further information regarding EPA drinking water models used in pesticide exposure assessment can be found at http://www2.epa.gov/pesticide-science-and-assessing-pesticide-risks/a bout-water-exposure-models-used-pesticide.

Tier 1 (Rice Model) Estimated Drinking Water Co ncentrations (EDWCs) in surface and groundwater for NAA were used in the dietary exposure assessment. The EDWCs were calculated using the Tier 1 surface water aquatic model First Index Reservoir Screening tool (FIRST) and the Tier I/II groundwater model Pesticide Root Zone Model Ground Water (PRZM GW), in Tier I mode. Accordingly, the EDWCs of NAA for chro nic exposures for non-cancer assessments are estimated to be 65.1 parts per billion (ppb) for surface water and 646 ppb for ground water.

Modeled estimates of drinking water co ncentrations were directly entered into the dietary exposure model. For chro nic dietary risk assessment, the water co ncentration value of 646 ppb was used to assess the co ntribution to drinking water.

3. From non-dietary exposure. The term “residential exposure” is used in this docu ment to refer to non-occupational, non-dietary exposure (e.g., for lawn and garden pest control, indoor pest control, termiticides, and flea and tick co ntrol on pets).

NAA is currently registered for root dip and sprout inhibition applications to ornamentals, which could result in residential exposures. There is a potential for short-term oral and inhalation exposures to residential handlers, resulting from loading and applying NAA. Though there is potential for dermal exposures for residential handlers, no dermal endpoint was selec ted due to the lack of systemic toxicity up to the limit dose (1,000 milligram/kilogram/day (mg/kg/day)). There are no residential uses for NAA that result in incidental dermal or oral exposure to children. The rooting compounds are applied by holding the plant and dipping the roots into solution. Very little exposure is expected from this use. Sprout inhibitors are applied by spray or paint brush/roller after pruning trees, or by spraying near the ba se of the tree after pruning root suckers. There is very little potential for post-application exposure to NAA for adults or children ba sed on the residential use pattern; therefore, residential post-application exposure is not expected, nor is intermediate- or long-term exposure ba sed on the intermittent nature of applications by homeowners.

Further information regarding EPA standard assumptions and generic inputs for residential exposures may be found at http://www2.epa.gov/pesticide-science-and-assessing-pesticide-risks/standard-operating-procedures-residential-pesticide.

4. Cumulative effects from substances with a common mechanism of toxicity. Section 408(b)(2)(D)(v) of FFDCA requires that, when co nsidering whether to establish, modify, or revoke a tolerance, the Agency co nsider “available information” co ncerning the cumulative effects of a particular pesticide's residues and “other substances that have a common mechanism of toxicity.”

EPA has not found NAA to share a common mechanism of toxicity with any other substances, and NAA does not appear to produce a toxic me tabolite produced by other substances. For the purposes of this tolerance action, therefore, EPA has assumed that NAA does not have a common mechanism of toxicity with other substances. For information regarding EPA's efforts to determine which chemicals have a common mechanism of toxicity and to e valuate the cumulative effects of such chemicals, see EPA's Web site at http://www2.epa.gov/pesticide-science-and-assessing-pesticide-risks/culmative-assessment-risk-pesticides.

D. Safety Factor for Infants and Children

1. In general. Section 408(b)(2)(C) of FFDCA provides that EPA shall apply an additio nal 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 databa se on toxicity and exposure unless EPA determines ba sed on reliable data that a different margin of safety will be safe for infants and children. This additio nal margin of safety is commo nly referred to as the Food Quality Protection Act Safety Factor (FQPA SF). In applying this provision, EPA either retains the default value of 10X, or uses a different additio nal safety factor when reliable data available to EPA support the choice of a different factor.

2. Prenatal and postnatal sensitivity. There is low co ncern and no residual uncertainty for pre- and/or postnatal toxicity resulting from exposure to the naphthalene acetates. Clear NOAELs and LOAELs were established for the developmental and offspring effects and the points of departure selec ted for all exposure scenarios are protective of these effects.

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 for the oral and dermal routes of exposure but retained a 10X for the inhalation route of exposure. That decision is ba sed on the following findings:

i. The toxicity databa se for NAA is complete, except for a subchro nic inhalation toxicity study. EPA is retaining a 10X FQPA SF for the inhalation route of exposure however, as discussed in Unit III.C.3, the EPA o nly expects short-term inhalation exposures to residential handlers, resulting from loading and applying NAA. Therefore, there is no co ncern for increased susceptibility in infants and children via the inhalation route. EPA waived the requirements for the acute and subchro nic neurotoxicity studies.

ii. There is no indication that NAA is a neurotoxic chemical ba sed on the available studies in the databa se, and EPA determined that there is no need for acute and subchro nic developmental neurotoxicity studies or additio nal UFs to account for neurotoxicity.

iii. The endpoints selec ted from the co-critical dog studies are protective of the effects observed in the rat developmental, rabbit developmental, and rat reproduction studies. Therefore, the potential for increased susceptibility in infants and children is low.

iv. There are no residual uncertainties identified in the exposure databa ses. The chro nic dietary food exposure assessment was performed ba sed on 100 PCT and tolerance-level residues. EPA made co nservative (protective) assumptions in the ground and surface water modeling used to assess exposure to NAA in drinking water. ba sed on the discussion in Unit III.C.3., regarding limited residential use patterns, exposure to residential handlers is very low and EPA does not anticipate post-application exposure to children or incidental dermal or oral exposures to toddlers resulting from use of NAA in residential settings. These assessments will not underestimate the exposure and risks posed by NAA.

E. Aggregate Risks and Determination of Safety

EPA determines whether acute and chro nic dietary pesticide exposures are safe by comparing aggregate exposure estimates to the acute PAD (aPAD) and chro nic 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 e valuated 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 co nsumption of food and drinking water. No adverse effect resulting from a single oral exposure was identified and no acute dietary endpoint was selec ted. Therefore, NAA is not expected to pose an acute risk.

2. Chro nic risk. Using the exposure assumptions described in this unit for chro nic exposure, EPA has co ncluded that chro nic exposure to NAA from food and water will utilize 15% of the cPAD for infants <1 year old the population group receiving the greatest exposure. ba sed on the explanation in Unit III.C.3., regarding residential use patterns, chro nic residential exposure to residues of NAA is not expected.

3. Short-term risk. Short-term aggregate exposure takes into account short-term residential exposure plus chro nic exposure to food and water (co nsidered to be a background exposure level). Using the exposure assumptions described in this unit for short-term exposures, short-term aggregate risk was estimated for combined oral and inhalation exposure in adults applying naphthalene acetate products with a paint-airless sprayer. This is co nsidered the worst case scenario for the aggregate risk assessment. Endpoints selec ted for the short-term adult oral exposure and inhalation exposure were ba sed on common effects and could therefore be combined in the aggregate assessment.

The EPA calculated an aggregated risk indices (ARI) to combine inhalation and oral exposures to adults. This resulted in an ARI greater than 1. An ARI value greater than 1 is not of co ncern to EPA, therefore, aggregate exposure to residential handlers is acceptable.

4. Intermediate-term risk. Intermediate-term aggregate exposure takes into account intermediate-term residential exposure plus chro nic exposure to food and water (co nsidered to be a background exposure level). Because no intermediate-term adverse effect was identified, NAA is not expected to pose an intermediate-term risk.

5. Aggregate cancer risk for U.S. population. ba sed on the lack of evidence of carcinogenicity in two adequate rodent carcinogenicity studies, NAA is not expected to pose a cancer risk to humans.

6. Determination of safety. ba sed on these risk assessments, EPA co ncludes that there is a reaso nable certainty that no harm will result to the general population, or to infants and children from aggregate exposure to NAA residues.

IV. Other Considerations

A. Analytical Enforcement Methodology

Adequate enforcement methodology, a high performance liquid chromatography (HPLC) method using fluorescence detection (Method NAA-AM-001) and a similar method (Method NAA-AM-002), is available to enforce the tolerance ex pression for NAA in plant commodities.

The method may be requested from: Chief, Analytical Chemistry Branch, Enviro nmental Science Center, 701 Mapes Rd., Ft. Meade, MD 20755-5350; telephone number: (410) 305-2905; email address: residuemethods@epa.gov.

B. Internatio nal Residue Limits

In making its tolerance decisions, EPA seeks to harmo nize U.S. tolerances with internatio nal standards whenever possible, co nsistent with U.S. food safety standards and agricultural practices. EPA co nsiders the internatio nal 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 internatio nal 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.

There is no established Codex MRL for NAA use on pomegranate.

V. Conclusion

Therefore, a tolerance is established for residues of NAA in or on pomegranate at 0.05 ppm.