[Federal Register Volume 63, Number 157 (Friday, August 14, 1998)]
[Rules and Regulations]
[Pages 43629-43637]
From the Federal Register Online via the Government Publishing Office [www.gpo.gov]
[FR Doc No: 98-21893]


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 ENVIRONMENTAL PROTECTION AGENCY

40 CFR Part 180

[OPP-300693A; FRL-6021-9]
RIN 2070-AB78


Spinosad; Pesticide Tolerance

AGENCY: Environmental Protection Agency (EPA).

ACTION: Final rule.

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SUMMARY: This regulation establishes a time-limited tolerance for 
residues of spinosad in or on coffee at 0.02 parts per million (ppm). 
This action is being initiated by EPA under the Federal Food, Drug and 
Cosmetic Act (FFDCA), as amended by the Food Quality Protection Act of 
1996 (Pub. L. 104-170). The United States Department of Agriculture/
Agricultural Research Service (USDA/ARS) has requested that EPA 
establish a time-limited tolerance on coffee in order for USDA/ARS to 
conduct efficacy testing of spinosad to control the Mediterranean Fruit 
Fly. This testing will be conducted on 80 acres in Hawaii under an 
Experimental Use Permit (EUP).

DATES: This regulation is effective August 14, 1998. Objections and 
requests for hearings must be received by EPA on or before Ocotber 13, 
1998.

ADDRESSES: Written objections and hearing requests, identified by the 
docket control number, [OPP-300693A], must be submitted to: Hearing 
Clerk (1900), Environmental Protection Agency, Rm M3708, 401 M St., 
SW., Washington, DC 20460. Fees accompanying objections and hearing 
requests shall be labeled ``Tolerance Petition Fees'' and forwarded to: 
EPA Headquarters Accounting Operations Branch, OPP (Tolerance Fees, 
P.O. Box 360277M, Pittsburgh, PA 15251. A copy of any objections and 
hearing requests

[[Page 43630]]

filed with the Hearing Clerk identified by the docket control number, 
[OPP-300693A], must also be submitted to: Public Information and 
Records Integrity Branch, Information Resources and Services Division 
(7502C), Office of Pesticide Programs, Environmental Protection Agency, 
401 M St., SW., Washington, DC 20460. In person bring comments to: Rm. 
119, CM #2, 1921 Jefferson Davis Highway, Arlington, VA.
    A copy of objections and hearing requests filed with the Hearing 
Clerk may also be submitted electronically to: opp-
[email protected]. Copies of objections and hearing requests must 
be submitted as an ASCII file avoiding the use of special characters 
and any form of encryption. Copies of objections and hearing requests 
will also be accepted on disks in WordPerfect 5.1/6.1 file format or 
ASCII file format. All copies of objections and hearing requests in 
electronic form must be identified by the docket control number [OPP-
300693A]. No confidential business information (CBI) should be 
submitted through e-mail. Electronic copies of objections and hearing 
requests on this rule may be filed online at many Federal Depository 
Libraries.

FOR FURTHER INFORMATION CONTACT: By mail: Susan Lewis, Registration 
Division [7505C], Office of Pesticide Programs, Environmental 
Protection Agency, 401 M St., SW., Washington, DC 20460. Office 
location, telephone number, and e-mail address: Crystal Mall #2, 1921 
Jefferson Davis Hwy., Arlington, VA, (703) 305-7448, e-mail: 
[email protected].

SUPPLEMENTARY INFORMATION: In the Federal Register of April 15, 1998 
(63 FR 18329)(FRL-5785-7), EPA established permanent tolerances by 
removing the time limitation for the tolerance for residues of the 
insecticide spinosad in or on cottonseed at 0.02 ppm and by 
establishing tolerances in or on almonds at 0.02 ppm; almond hulls at 
2.0 ppm; apples at 0.2 ppm; apple pomace, wet at 0.5 ppm; citrus fruits 
group at 0.3 ppm; dried citrus pulp at 0.5 ppm; citrus oil at 3.0 ppm; 
cotton gin byproducts at 1.5 ppm; fruiting vegetables (except 
cucurbits) group at 0.4 ppm; leafy vegetables (except Brassica 
vegetables) group at 8.0 ppm; Brassica (cole), leafy vegetables, head 
and stem subgroup at 2.0 ppm; Brassica (cole), leafy vegetables, greens 
subgroup at 15.0 ppm; fat of cattle, goats, hogs, horses, and sheep at 
0.7 ppm; meat of cattle, goats, hogs, horses, and sheep at 0.04 ppm; 
meat byproducts of cattle, goats, hogs, horses, and sheep at 0.2 ppm; 
milk fat at 0.5 ppm; and whole milk at 0.04 ppm.
    In the Federal Register of July 28, 1998 (63 FR 40239)(FRL-6020-6), 
EPA issued a proposed rule announcing the request for a time-limited 
tolerance on coffee by USDA/ARS. There were no comments received in 
response to the proposed rule.
    The USDA has requested that EPA establish a time-limited tolerance 
for residues of spinosad in or on coffee. USDA has requested this 
tolerance in order to conduct efficacy testing of spinosad for control 
of the Mediterranean Fruit Fly. This testing will be conducted on 80 
acres in Hawaii under an Experimental Use Permit (EUP).
    The Agency has concluded that a tolerance of 0.02 ppm (which is the 
Limit of Quantitation (LOQ) for the analytical method) is adequate for 
coffee. This is based on a very low application rate and the fact that 
the hull of the coffee bean is removed. No residues are expected to be 
found on the coffee beans. The tolerance will expire on August 28, 
2000.

I. Risk Assessment and Statutory Findings

    New section 408(b)(2)(A)(i) of the 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) 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) 
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. . . .''
    EPA performs a number of analyses to determine the risks from 
aggregate exposure to pesticide residues. First, EPA determines the 
toxicity of pesticides based primarily on toxicological studies using 
laboratory animals. These studies address many adverse health effects, 
including (but not limited to) reproductive effects, developmental 
toxicity, toxicity to the nervous system, and carcinogenicity. Second, 
EPA examines exposure to the pesticide through the diet (e.g., food and 
drinking water) and through exposures that occur as a result of 
pesticide use in residential settings.

A. Toxicity

    1. Threshold and non-threshold effects. For many animal studies, a 
dose response relationship can be determined, which provides a dose 
that causes adverse effects (threshold effects) and doses causing no 
observed effects (the ``no-observed effect level'' or ``NOEL'').
    Once a study has been evaluated and the observed effects have been 
determined to be threshold effects, EPA generally divides the NOEL from 
the study with the lowest NOEL by an uncertainty factor (usually 100 or 
more) to determine the Reference Dose (RfD). The RfD is a level at or 
below which daily aggregate exposure over a lifetime will not pose 
appreciable risks to human health. An uncertainty factor (sometimes 
called a ``safety factor'') of 100 is commonly used since it is assumed 
that people may be up to 10 times more sensitive to pesticides than the 
test animals, and that one person or subgroup of the population (such 
as infants and children) could be up to 10 times more sensitive to a 
pesticide than another. In addition, EPA assesses the potential risks 
to infants and children based on the weight of the evidence of the 
toxicology studies and determines whether an additional uncertainty 
factor is warranted. Thus, an aggregate daily exposure to a pesticide 
residue at or below the RfD (expressed as 100 percent or less of the 
RfD) is generally considered acceptable by EPA. EPA generally uses the 
RfD to evaluate the chronic risks posed by pesticide exposure. For 
shorter term risks, EPA calculates a margin of exposure (MOE) by 
dividing the estimated human exposure into the NOEL from the 
appropriate animal study. Commonly, EPA finds MOEs lower than 100 to be 
unacceptable. This hundredfold MOE is based on the same rationale as 
the hundredfold uncertainty factor.
    Lifetime feeding studies in two species of laboratory animals are 
conducted to screen pesticides for cancer effects. When evidence of 
increased cancer is noted in these studies, the Agency conducts a 
weight of the evidence review of all relevant toxicological data 
including short-term and mutagenicity studies and structure activity 
relationship. Once a pesticide has been classified as a potential human 
carcinogen, different types of risk assessments (e.g., linear low dose 
extrapolations or MOE calculation based on the appropriate NOEL) will 
be carried out based on the nature of the

[[Page 43631]]

carcinogenic response and the Agency's knowledge of its mode of action.
    2. Differences in toxic effect due to exposure duration. The 
toxicological effects of a pesticide can vary with different exposure 
durations. EPA considers the entire toxicity data base, and based on 
the effects seen for different durations and routes of exposure, 
determines which risk assessments should be done to assure that the 
public is adequately protected from any pesticide exposure scenario. 
Both short and long durations of exposure are always considered. 
Typically, risk assessments include ``acute,'' ``short-term,'' 
``intermediate term,'' and ``chronic'' risks. These assessments are 
defined by the Agency as follows.
    Acute risk, by the Agency's definition, results from 1-day 
consumption of food and water, and reflects toxicity which could be 
expressed following a single oral exposure to the pesticide residues. 
High end exposure to food and water residues are typically assumed.
    Short-term risk results from exposure to the pesticide for a period 
of 1-7 days, and therefore overlaps with the acute risk assessment. 
Historically, this risk assessment was intended to address primarily 
dermal and inhalation exposure which could result, for example, from 
residential pesticide applications. However, since enaction of FQPA, 
this assessment has been expanded to include both dietary and non-
dietary sources of exposure, and will typically consider exposure from 
food, water, and residential uses when reliable data are available. In 
this assessment, risks from average food and water exposure, and high-
end residential exposure, are aggregated. High-end exposures from all 
three sources are not typically added because of the very low 
probability of this occurring in most cases, and because the other 
conservative assumptions built into the assessment assure adequate 
protection of public health. However, for cases in which high-end 
exposure can reasonably be expected from multiple sources (e.g. 
frequent and widespread homeowner use in a specific geographical area), 
multiple high-end risks will be aggregated and presented as part of the 
comprehensive risk assessment/characterization. Since the toxicological 
endpoint considered in this assessment reflects exposure over a period 
of at least 7 days, an additional degree of conservatism is built into 
the assessment; i.e., the risk assessment nominally covers 1-7 days 
exposure, and the toxicological endpoint/NOEL is selected to be 
adequate for at least 7 days of exposure. (Toxicity results at lower 
levels when the dosing duration is increased.)
    Intermediate-term risk results from exposure for 7 days to several 
months. This assessment is handled in a manner similar to the short-
term risk assessment.
    Chronic risk assessment describes risk which could result from 
several months to a lifetime of exposure. For this assessment, risks 
are aggregated considering average exposure from all sources for 
representative population subgroups including infants and children.

B. Aggregate Exposure

    In examining aggregate exposure, FFDCA section 408 requires that 
EPA take into account available and reliable information concerning 
exposure from the pesticide residue in the food in question, residues 
in other foods for which there are tolerances, residues in groundwater 
or surface water that is consumed as drinking water, and other non-
occupational exposures through pesticide use in gardens, lawns, or 
buildings (residential and other indoor uses). Dietary exposure to 
residues of a pesticide in a food commodity are estimated by 
multiplying the average daily consumption of the food forms of that 
commodity by the tolerance level or the anticipated pesticide residue 
level. The Theoretical Maximum Residue Contribution (TMRC) is an 
estimate of the level of residues consumed daily if each food item 
contained pesticide residues equal to the tolerance. In evaluating food 
exposures, EPA takes into account varying consumption patterns of major 
identifiable subgroups of consumers, including infants and children. 
The TMRC is a ``worst case'' estimate since it is based on the 
assumptions that food contains pesticide residues at the tolerance 
level and that 100% of the crop is treated by pesticides that have 
established tolerances. If the TMRC exceeds the RfD or poses a lifetime 
cancer risk that is greater than approximately one in a million, EPA 
attempts to derive a more accurate exposure estimate for the pesticide 
by evaluating additional types of information (anticipated residue data 
and/or percent of crop treated data) which show, generally, that 
pesticide residues in most foods when they are eaten are well below 
established tolerances.

II. Aggregate Risk Assessment and Determination of Safety

    Consistent with section 408(b)(2)(D), EPA has reviewed the 
available scientific data and other relevant information in support of 
the existing uses of spinosad. EPA had sufficient data to assess the 
hazards of spinosad and to make a determination on aggregate exposure, 
consistent with section 408(b)(2), for tolerances for residues of 
spinosad for those uses. EPA's assessment of the dietary exposures and 
risks associated with establishing the existing tolerances 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 nature of the toxic effects caused by spinosad are 
discussed below.
    1. Acute toxicity studies with technical spinosad (88% - 90.4%): 
Oral LD50 in the rat is > 5,000 milligram/kilogram (mg/kg) 
for males and females - Toxicity Category IV; dermal LD50 in 
the rat is > 2,800 mg/kg for males and females - Toxicity Category III; 
inhalation LC50 in the rat is > 5.18 mg/L - Toxicity 
Category IV; primary eye irritation in the rabbit (slight conjunctival 
irritation) - Toxicity Category IV; primary dermal irritation in the 
rabbit (no erythema and edema) - Toxicity Category IV. Spinosad is not 
a sensitizer.
    2. Acute toxicity studies with the end-use (44% formulation) 
product for spinosad: Oral LD50 in the rat is > 5,000 mg/kg 
for males and females - Toxicity Category IV; dermal LD50 in 
the rat is > 2,800 mg/kg for males and females - Toxicity Category III; 
inhalation LC50 in the rat is > 5 mg/L - Toxicity Category 
IV; primary eye irritation in the rabbit (slight conjunctival 
irritation) - Toxicity Category IV; primary dermal irritation in the 
rabbit (slight transient erythema and edema) - Toxicity Category IV; 
not a sensitizer.
    3. In a subchronic feeding study in rats, the no-observed adverse 
effect level (NOAEL) was 33.9 and 38.8 mg/kg/day for males and females, 
respectively. The lowest observed effect level (LOEL) was 68.5 and 78.1 
mg/kg/day for males and females, respectively based on decreased body 
weight gain, anemia, and vacuolation in multiple organs (kidney, liver, 
heart, spleen, adrenals, and thyroid).
    4. In a subchronic feeding study in mice, the no observed effect 
level (NOEL) was 7.5 mg/kg/day and the LOEL was 22.5 mg/kg/day based on 
cytoplasmic vacuolation in multiple

[[Page 43632]]

organs (kidney, liver, heart, stomach, lymphoid organs, and ovary).
    5. In a subchronic feeding study in dogs, the NOEL was 4.89 and 
5.38 mg/kg/day for males and females, respectively. The LOEL was 9.73 
mg/kg/day and 10.5 mg/kg/day based on decreased mean body weights and 
food consumption, and anemia.
    6. In a 21-day dermal study in rats, the NOEL for systemic effects 
was > 1,000 mg/kg/day (limit dose). No systemic toxicity was observed 
at any dose tested.
    7. In a chronic feeding study in dogs, the NOEL was 2.68 mg/kg/day. 
The LOEL was 8.22 mg/kg/day based on increased liver enzymes (ALT, 
AST), triglycerides; vacuolated cells (parathyroid), and arteritis.
    8. In an carcinogenicity study in mice, the NOEL was 11.4 mg/kg/
day. The LOEL was 50.9 mg/kg/day based on decreased body weight gains, 
increased mortality, hematologic effects, increased thickening of the 
gastric mucosa, and histologic changes in the stomach of males.
    9. In a chronic feeding/carcinogenicity/neurotoxicity study in 
rats, the NOEL (systemic) was 9.5 and 12.0 mg/kg/day for males and 
females, respectively. The LOEL (systemic) was 24.1 and 30.3 mg/kg/day 
for males and females, respectively based on vacuolation of epithelial 
follicular cells of the thyroid. The neurological NOEL was 46 and 57 
mg/kg/day for males and females, respectively. The neurological LOEL 
was not determined.
    10. In a developmental study in rabbits, the maternal NOEL was 
 50 mg/kg/day. The maternal LOEL was not established. The 
developmental NOEL was  50 mg/kg/day. The developmental LOEL 
was not established.
    11. In a developmental study in rats, the maternal NOEL was > 200 
mg/kg/day. The maternal LOEL was not established. The developmental 
NOEL was > 200 mg/kg/day. The developmental LOEL was not established.
    12. In a two-generation reproduction toxicity study in rats, the 
systemic NOEL was 10 mg/kg/day. The systemic LOEL was 100 mg/kg/day 
based on increased organ weights (heart, liver, kidney, spleen, 
thyroid), histopath lesions in the lungs and mesenteric lymph nodes, 
stomach (F), and prostate. The reproductive NOEL was 10 mg/kg/day. The 
reproductive LOEL was 100 mg/kg/day based on decreased litter size, 
decreased pup survival, decreased body weight, increased incidence of 
dystocia and/or vaginal bleeding post-partum with associated increased 
mortality of dams.
    13. Studies on gene mutation and other genotoxic effects: In a Gene 
Mutation Assay (mouse forward mutation) there was no forward mutation 
induction in mouse lymphoma L5178Y Tk +/- cells at concentrations of 0, 
1, 5, 10, 15, 20, or 25 g/ml without metabolic activation or 
at concentrations of 15 through 50 g/ml with metabolic 
activation. In a Structural Chromosomal Aberration Assay In vitro there 
was no increase in the number of CHO (chinese hamster ovary) cells with 
chromosomal aberrations at concentrations from 20 to 35 g/ml 
(without activation) or concentrations from 100 to 500 g/ml 
(with activation). In a Micronucleus Test in mice, there was no 
increase in the frequencey of micronuclei in bone marrow cells from 
mice treated at concentrations from 500 to 2,000 g/ml for 2 
days. In Other Genotoxicity Assays, unscheduled DNA synthesis was not 
induced in adult rat hepatocytes in vitro at concentrations of 0.01 to 
5 g/ml tested.
    14. The results of three metabolism studies are as follows: i. 
Approximately 95% of technical spinosad was eliminated by 24 hours 
mainly in the urine (34%), bile (36%), and tissues and carcass (21%). 
Metabolites include the glutathione conjugates of the unchanged form as 
well as N- and O-demethylated forms of XDE-105 (Factor D).
    ii. At 100 mg/kg/dose, the radiolabeled XDE-105 (Factor D) was 
primarily excreted in the feces (68%) after 24-hours. The absorption, 
distribution, and elimination of 14C-XDE-105 (Factor A) demonstrated no 
appreciable differences based on dose or repeated dosing.
    iii. At high (100 mg/kg) doses, there are no major differences in 
the bioavailability, routes or rates of excretion or metabolism of 14C-
XDE-105 (Factor A) following oral administration.
    15. In an acute neurotoxicity study, groups of Fischer 334 rats 
(10/sex/dose) received a single oral (gavage) administration of 
spinosad (87.9%) at dose levels of 0, 200, 630, or 2,000 mg/kg. There 
were no effects on neurobehavioral endpoints or histopathology of the 
nervous system. For neurotoxicity, the NOEL was  2,000 mg/
kg/day (HDT). A LOEL was not established.
    16. In a subchronic neurotoxicity study, groups of Fischer 344 rats 
(10/sex/dose) were administered diets containing spinosad at levels of 
0, 0.003, 0.006, 0.012, or 0.06% (0, 2.2, 4.3, 8.6, or 42.7 mg/kg/day 
for males and 2.6, 5.2, 10.4, or 52.1 mg/kg/day for females, 
respectively). There were no effects on neurobehavior endpoints or 
histopathology of the nervous system. For neurotoxicity, the NOEL was 
 42.7 and  52.1 mg/kg/day in males and females, 
respectively (HDT).
    17. In the 2-year chronic neurotoxicity study, groups of Fischer 
344 rats (65/sex/dose) received diets containing spinosad at dose 
levels of 0, 0.005, 0.02, 0.05, or 0.1% (0, 2.4, 9.5, 24.1, or 49.4 mg/
kg/day for males and 0, 3.0, 12.0, 30.3, or 62.2 mg/kg/day for females, 
respectively). Neurobehavioral testing performed at 3, 6, 9, and 12 
months of study was negative, and histopathological evaluation of 
perfused tissues at study termination did not identify pathology of the 
central or peripheral nervous system. There was no evidence of 
neurotoxicity. For neuropathology, the NOEL was 0.1% ( 46 
mg/kg/day for males and 57 mg/kg/day for females (HDT).

B. Toxicological Endpoints

    1. Acute toxicity. EPA did not select a dose and endpoint for an 
acute dietary risk assessment due to the lack of toxicological effects 
attributable to a single exposure (dose) in studies available in the 
data base including oral developmental toxicity studies in rats and 
rabbits. In the acute neurotoxicity study the NOEL was  
2,000 mg/kg/day.
     2. Short - (1 day to 7 days), intermediate- (1 week to several 
months), and chronic - term occupational and residential dermal and 
inhalation toxicity. EPA did not select a dose or endpoint for short-, 
intermediate and long-term dermal risk assessments because (i) lack of 
appropriate endpoints; (ii) the combination of molecular structure and 
size as well as the lack of dermal or systemic toxicity at 2,000 mg/kg/
day in a 21-day dermal toxicity study in rats which indicates the lack 
of dermal absorption; and (iii) the lack of long-term exposure based on 
the current use pattern. Therefore, a dermal risk assessment is not 
required. EPA also determined that based on the current use pattern and 
exposure scenario, and inhalation risk assessment is not required.
     3. Chronic toxicity. EPA has established the RfD for spinosad at 
0.027 mg/kg/day. This RfD is based on a chronic toxicity study in dogs 
using a NOEL of 2.68 mg/kg/day. The LOEL was 8.46 mg/kg/day based on 
vacuolation in glandular cells (parathyroid) and lymphatic tissues, 
arteritis and increases in serum enzymes such as alanine 
aminotransferase, and aspartate

[[Page 43633]]

aminotransferase, and triglyceride levels in dogs fed spinosad in the 
diet at dose levels of 1.44, 2.68, or 8.46 mg/kg/day for 52 weeks. A 
hundredfold uncertainty factor (UF) was applied to the NOEL of 2.68 mg/
kg/day to account for inter- and intra-species variation.
    EPA determined that the 10X factor to account for enhanced 
sensitivity of infants and children (as required by FQPA) should be 
removed. Thus, an uncertainty factor of 100 is adequate and the RfD 
remains at 0.027 mg/kg/day.
    The FQPA factor is removed because: (i) the data provided no 
indication of increased susceptibility of rats or rabbits to in utero 
and/or post-natal exposure to spinosad. In the prenatal developmental 
toxicity studies in rats and rabbits and the two-generation 
reproduction study in rats, effects in the offspring were observed only 
at or below treatment levels which resulted in evidence of parental 
toxicity. (ii) No neurotoxic signs have been observed in any of the 
standard required studies conducted. (iii) The toxicology data base is 
complete and there are no data gaps.
    4. Carcinogenicity. There is no evidence of carcinogenicity in 
studies in either the mouse or rat.

C. Exposures and Risks

    1. From food and feed uses. Tolerances have been established (40 
CFR 180.495) for the residues of spinosad in or on almonds at 0.02 ppm; 
almond hulls at 2.0 ppm; apples at 0.2 ppm; apple pomace, wet at 0.5 
ppm; citrus fruits group at 0.3 ppm; dried citrus pulp at 0.5 ppm; 
citrus oil at 3.0 ppm; cottonseed at 0.02 ppm; cotton gin byproducts at 
1.5 ppm; fruiting vegetables (except cucurbits) group at 0.4 ppm; leafy 
vegetables (except Brassica vegetables) group at 8.0 ppm; Brassica 
(cole), leafy vegetables, head and stem subgroup at 2.0 ppm; Brassica 
(cole), leafy vegetables, greens subgroup at 15.0 ppm; fat of cattle, 
goats, hogs, horses, and sheep at 0.7 ppm; meat of cattle, goats, hogs, 
horses, and sheep at 0.04 ppm; meat byproducts of cattle, goats, hogs, 
horses, and sheep at 0.2 ppm; milk fat at 0.5 ppm; and whole milk at 
0.04 ppm.
    For the existing uses referred to above, risk assessments were 
conducted by EPA to assess dietary exposures and risks from spinosad as 
follows:
    i.  Acute exposure and risk. Acute dietary 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. No acute toxicological endpoints were 
identified for spinosad due to the lack of toxicological effects 
attributable to a single exposure (dose). Therefore, the Agency 
concludes that there is a reasonable certainty of no harm from acute 
dietary exposure.
    ii. Chronic exposure and risk. The RfD used for the chronic dietary 
analysis is 0.027 mg/kg/day. In conducting this chronic dietary risk 
assessment, EPA made very conservative assumptions: 100% of citrus, 
almonds, apples, fruiting (except cucurbit) vegetables, Brassica leafy 
vegetables, leafy vegetables, cottonseed, and ruminant commodities 
having spinosad tolerances will contain spinosad residues and those 
residues will be at the level of the established tolerance. This 
results in an overestimate of human dietary exposure. Thus, in making a 
safety determination for this tolerance, EPA is taking into account 
this conservative exposure assessment.
    The existing spinosad tolerances resulted in a Theoretical Maximum 
Residue Contribution (TMRC) that is equivalent to the following 
percentages of the RfD: U.S. population (24% of RfD); nursing infants 
(< 1 year old)( 8% of RfD); non-nursing infants (< 1 year old) (24% of 
RfD); children (1-6 years old) (34% of RfD); children (7-12 years old) 
(29% of RfD); Northeast Region (25% of RfD); Western Region (27% of 
RfD); Non-Hispanic Blacks (27% of RfD); Non-Hispanic others (37% of 
RfD); females 13+ years, nursing (27% of RfD).
    The Agency believes that the addition of a 0.02 ppm tolerance for 
spinosad on coffee will only change the percent of the RfD used for any 
of the categories listed above by less than 1%. This is based on the 
fact that the use will be limited to 80 acres in Hawaii for 
experimental purposes for period of time not to exceed 2 years.
    2. From drinking water. The Agency has determined that spinosyns 
Factor A and Factor D are immobile in soil and will not leach into 
ground water. Based on structure/activity relationships, the Agency 
concluded that the spinosad metabolites/fermentation impurities 
(spinosyns Factor B, Factor B of D, Factor K, and other related 
Factors) were of no more toxicological concern than the two parent 
compounds (spinosyns Factor A and Factor D) and therefore, only these 
were considered in the drinking water assessment. EPA used the 
``Interim Approach for Addressing Drinking Water Exposure in Tolerance 
Decision Making'' issued on 11/17/97. Thus, the PRZM/EXAMS Models were 
run to produce estimates of spinosad in surface water. The primary use 
of these models is to provide a screen for sorting out pesticides for 
which OPP has a high degree of confidence that the true levels of the 
pesticide in drinking water will be less than the human health drinking 
water levels of concern (DWLOCs). A human health DWLOC is the 
concentration of a pesticide in drinking water which would result in 
acceptable aggregate risk, after having already factored in all food 
exposures and other non-occupational exposures for which OPP has 
reliable data. PRZM/EXAMS was used to conduct a Tier 2 surface water 
analysis. The Tier 2 estimated drinking water concentration (EEC) of 
spinosad from surface water sources is not likely to exceed 0.059 
g/l from use on apples, 0.092 g/l from use on 
Brassica vegetables, 0.065 g/l from use on cotton, and 0.075 
g/l from use on citrus.
    i. Acute exposure and risk. Because no acute dietary endpoint was 
determined, the Agency concludes that there is a reasonable certainty 
of no harm from acute exposure from drinking water.
    ii. Chronic exposure and risk. Based on the chronic dietary (food) 
exposure and using default body weights and water consumption figures, 
chronic drinking water levels of concern (DWLOC) were calculated. The 
chronic drinking water exposure and risk estimates are 0.019890 mg/kg/
day (690 g/l DWLOC) for the overall U.S. population; 0.01896 
mg/kg/day (570 g/l DWLOC) for females 13+ years, nursing; and 
0.016865 mg/kg/day (170 g/l DWLOC) for children age 1-6 years.
    3. From non-dietary exposure. There are no current residential uses 
for spinosad. However, the proposed use of a 0.5% spinosad product on 
structural lumber may have residential uses. This product is injected 
into drilled holes and then sealed after treatment. Due to the lack of 
toxicity endpoints (hazard) and minimal contact with the active 
ingredient during and after application, exposure to residential 
occupants is not expected.
    4. Cumulative exposure to substances with common mechanism of 
toxicity. Spinosad has not yet been grouped with any other insecticides 
into a class.
    Section 408(b)(2)(D)(v) 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.'' The Agency believes that ``available 
information'' in this context might include not only toxicity, 
chemistry, and exposure data, but also scientific policies and 
methodologies for

[[Page 43634]]

understanding common mechanisms of toxicity and conducting cumulative 
risk assessments. For most pesticides, although the Agency has some 
information in its files that may turn out to be helpful in eventually 
determining whether a pesticide shares a common mechanism of toxicity 
with any other substances, EPA does not at this time have the 
methodologies to resolve the complex scientific issues concerning 
common mechanism of toxicity in a meaningful way. EPA has begun a pilot 
process to study this issue further through the examination of 
particular classes of pesticides. The Agency hopes that the results of 
this pilot process will increase the Agency's scientific understanding 
of this question such that EPA will be able to develop and apply 
scientific principles for better determining which chemicals have a 
common mechanism of toxicity and evaluating the cumulative effects of 
such chemicals. The Agency anticipates, however, that even as its 
understanding of the science of common mechanisms increases, decisions 
on specific classes of chemicals will be heavily dependent on chemical 
specific data, much of which may not be presently available.
    Although at present the Agency does not know how to apply the 
information in its files concerning common mechanism issues to most 
risk assessments, there are pesticides as to which the common mechanism 
issues can be resolved. These pesticides include pesticides that are 
toxicologically dissimilar to existing chemical substances (in which 
case the Agency can conclude that it is unlikely that a pesticide 
shares a common mechanism of activity with other substances) and 
pesticides that produce a common toxic metabolite (in which case common 
mechanism of activity will be assumed).
    EPA does not have, at this time, available data to determine 
whether spinosad has a common mechanism of toxicity with other 
substances or how to include this pesticide in a cumulative risk 
assessment. Unlike other pesticides for which EPA has followed a 
cumulative risk approach based on a common mechanism of toxicity, 
spinosad does not appear to produce a toxic metabolite produced by 
other substances. For the purposes of these tolerance actions, 
therefore, EPA has not assumed that spinosad has a common mechanism of 
toxicity with other substances.

D. Aggregate Risks and Determination of Safety for U.S. Population

    Chronic risk. The following information is based on the review of 
the existing uses of spinosad: Using the TMRC exposure assumptions 
described above, EPA has concluded that aggregate exposure to spinosad 
from food will utilize 24% of the RfD for the U.S. population. For the 
most highly exposed populations subgroup, children (1-6 years old), 
chronic dietary (food only) exposure occupies 34% of the RfD. This is a 
conservative risk estimate for reasons described above. EPA generally 
has no concern for exposures below 100% of the RfD because the RfD 
represents the level at or below which daily aggregate dietary exposure 
over a lifetime will not pose appreciable risks to human health. The 
chronic DWLOC for the infants and children subgroup is 170 parts per 
billion (ppb). The chronic modeling estimates (EECs) for spinosad 
residues in surface water are as high as 0.092 ppb from use on Brassica 
leafy vegetables. The maximum estimated concentrations of spinosad in 
surface water are less than EPA's levels of concern for spinosad in 
drinking water as a contribution to chronic aggregate exposure. Taking 
into account present uses and uses proposed in this risk assessment, 
EPA concludes with reasonable certainty that residues of spinosad in 
drinking water (when considered along with other sources of exposure 
for which EPA has reliable data ) would not result in unacceptable 
levels of aggregate human health risk at this time. Therefore, the 
Agency concludes that there is a reasonable certainty that no harm will 
result from chronic aggregate exposure to spinosad residues from food 
and water.
    No dermal or inhalation endpoints were identified. Due to the 
nature of the non-dietary use, EPA believes that the use of spinosad in 
treating structural lumber will not result in any exposure through the 
oral route. Therefore, the chronic aggregate risk is the sum of food 
and water.
    Based on the above information, the Agency concludes that there is 
a reasonable certainty that no harm will result from chronic aggregate 
exposure to spinosad from food and water resulting from the addition of 
the time-limited experimental use on coffee as described above.

E. Aggregate Cancer Risk for U.S. Population

    The RfD Committee determined that there is no evidence of 
carcinogenicity in studies in either the mouse or rat. Therefore, a 
carcinogenic risk assessment is not required.

F. Aggregate Risks and Determination of Safety for Infants and Children

    1. Safety factor for infants and children-- a. In general. In 
assessing the potential for additional sensitivity of infants and 
children to residues of spinosad, EPA considered data from 
developmental toxicity studies in the rat and rabbit and a two-
generation reproduction study in the rat. The developmental toxicity 
studies are designed to evaluate adverse effects on the developing 
organism resulting from pesticide exposure during prenatal development 
to one or both parents. Reproduction studies provide information 
relating to effects from exposure to the pesticide on the reproductive 
capability of mating animals and data on systemic toxicity.
    FFDCA section 408 provides that EPA shall apply an additional 
tenfold margin of safety for infants and children in the case of 
threshold effects to account for pre-and post-natal toxicity and the 
completeness of the database unless EPA determines that a different 
margin of safety will be safe for infants and children. Margins of 
safety are incorporated into EPA risk assessments either directly 
through use of a MOE analysis or through using uncertainty (safety) 
factors in calculating a dose level that poses no appreciable risk to 
humans. EPA believes that reliable data support using the standard MOE 
and uncertainty factor (usually 100 for combined inter- and intra-
species variability) and not the additional tenfold MOE/uncertainty 
factor when EPA has a complete data base under existing guidelines and 
when the severity of the effect in infants or children or the potency 
or unusual toxic properties of a compound do not raise concerns 
regarding the adequacy of the standard MOE/safety factor.
    b. Developmental toxicity studies. i. In a prenatal developmental 
toxicity study, groups of pregnant Sprague-Dawley rats (30/group) 
received oral (gavage) administration of spinosad (88.6%) in aqueous 
0.5% methycellulose at dose levels of 0, 10, 50, 200 mg/kg/day during 
gestation days 6 through 17. For maternal toxicity, the NOEL was 
 200 mg/kg/day (HDT); a LOEL was not established. Marginal 
maternal toxicity was reported at this dose level (decreased body 
weight gain). Based upon the results of a range-finding study, which 
showed maternal toxicity (body weight and food consumption decreases at 
100 and 300 mg/kg/day), the dose level of 200 mg/kg/day in the main 
study was considered adequate. For developmental toxicity, the NOEL was 
> 200 mg/kg/day; a LOEL was not

[[Page 43635]]

established. In the range-finding study, fetal body weight decrements 
occurred at 300 mg/kg/day.
    ii. In a prenatal developmental toxicity study, groups of pregnant 
New Zealand White rabbits (20/group) received oral (gavage) 
administration of spinosad (88.6%) in 0.5% aqueous methyl cellulose at 
doses of 0, 2.5, 10, or 50 mg/kg/day during gestation days 7 through 
19. For maternal toxicity, the NOEL was  50 mg/kg/day (HDT); 
a LOEL was not established. At this dose, slight body weight loss was 
observed in the first few days of dosing, but this finding was not 
supported by other signs. In the range-finding study, inanition was 
observed at doses of 100, 200, and 400 mg/kg/day, with significant 
decreases in body weight gain during dosing. All does at these dose 
levels were sacrificed prior to scheduled termination; no fetal data 
were available. No evidence of developmental toxicity was noted. For 
developmental toxicity, the NOEL was  50 mg/kg/day; a LOEL 
was not established. (No fetal effects were noted for fetuses of the 
range-finding study at doses up to 50 mg/kg/day).
    c. Reproductive toxicity study. In a two-generation reproduction 
study, groups of Sprague-Dawley rats (30/sex/group) received diets 
containing spinosad (88%) at dose levels of 0, 0.005, 0.02, or 0.2% (3, 
10, or 10 mg/kg/day, respectively) for two successive generations. For 
parental systemic toxicity, the NOEL was 0.02% (10 mg/kg/day) and the 
LOEL was 0.2% (100 mg/kg/day), based on increased heart, kidney, liver, 
spleen, and thyroid weights (both sexes), histopathology in the spleen 
and thyroid (both sexes), heart and kidney (males), and histopathologic 
lesions in the lungs and mesenteric lymph nodes (both sexes), stomach 
(females), and prostate. For offspring toxicity, the NOEL was 0.02% (10 
mg/kg/day) and the LOEL was 0.2% (100 mg/kg/day) based on decreased 
litter size, survival (F2), and body weights. Reproductive effects at 
that dose level included increased incidence of dystocia and/or vaginal 
bleeding after parturition with associated increase in mortality of 
dams.
    d. Neurotoxicity. i. In an acute neurotoxicity study, groups of 
Fischer 344 rats (10/sex/dose) received a single oral (gavage) 
administration of spinosad (87.9%) at dose levels of 0, 200, 630, or 
2,000 mg/kg. There were no effects on neurobehavioral endpoints or 
histopathology of the nervous system. For neurotoxicity, the NOEL was > 
2,000 mg/kg (HDT); a LOEL was not established.
    ii. In a subchronic neurotoxicity study, groups of Fisher 344 rats 
(10/sex/dose) were administered diets containing spinosad at levels of 
0, 0.003, 0.006, 0.012, or 0.06% (0, 2.2, 4.3, 8.6, or 42.7 mg/kg/day 
for males and 2.6, 5.2, 10.4, or 52.1 mg/kg/day for females, 
respectively). There were no effects on neurobehavioral endpoints or 
histopathology of the nervous system. For neurotoxicity, the NOEL was 
 42.7 for males and  52.1 mg/kg/day for females 
(HDT).
    iii. In the 2-year chronic toxicity study, groups of Fischer 344 
rats (65/sex/dose) received diets containing spinosad at dose levels of 
0, 0.005, 0.02, 0.05, or 0.1% (0, 2.4, 9.5, 24.1, or 49.4 mg/kg/day for 
males and 0, 3.0, 12.0, 30.3, or 62.2 mg/kg/day for females, 
respectively). Neurobehavioral testing performed at 3, 6, 9, and 12 
months of study was negative, and histopathological evaluation of 
perfused tissues at study termination did not identify pathology of the 
central or peripheral nervous system. There was no evidence of 
neurotoxicity. For neuropathology, the NOEL was 0.1% (> 49.4 mg/kg/day 
for males and 62.8 mg/kg/day for females).
    e. Pre- and post-natal sensitivity. There was no increased 
susceptibility to rats or rabbits following in utero and/or postnatal 
exposure to spinosad.
     f. Conclusion. The data provided no indication of increased 
susceptibility of rats or rabbits to in utero and/or postnatal exposure 
to spinosad. In the prenatal developmental toxicity studies in rats and 
rabbits and the two-generation reproduction study in rats, effects in 
the offspring were observed only at or below treatment levels which 
resulted in evidence of parental toxicity. In addition, all 
neurotoxicity studies were negative for effects on the central or 
peripheral nervous system.
    EPA determined that the 10X factor to account for enhanced 
sensitivity of infants and children (as required by FQPA) should be 
removed. The FQPA factor is removed because (i) the data provided no 
indication of increased susceptibility of rats or rabbits to in utero 
and/or post natal exposure to spinosad. In the prenatal developmental 
toxicity studies in rats and rabbits and the two-generation 
reproduction study in rats, effects in the offspring were observed only 
at or below treatment levels which resulted in evidence of parental 
toxicity. (ii) No neurotoxic signs have been observed in any of the 
standard required studies conducted. (iii) The toxicology data base is 
complete and there are no data gaps.
    2. Acute risk. An acute risk assessment is not required because no 
acute toxicological endpoints were identified for spinosad.
    3. Chronic risk. Using the conservative exposure assumptions 
described above, EPA has concluded that aggregate exposure to spinosad 
from food will utilize 34% of the RfD for children age 1-6 years old. 
EPA generally has no concern for exposures below 100% of the RfD 
because the RfD represents the level at or below which daily aggregate 
dietary exposure over a lifetime will not pose appreciable risks to 
human health. EPA concludes that there is a reasonable certainty that 
no harm will result to infants and children from aggregate exposure to 
spinosad residues.
    Based on the above information, EPA concludes that there is a 
resonable certainty that no harm will result to infants and children 
from aggregate exposure to spinosad residues as a result of the use on 
coffee in an experimental use program in Hawaii.

G. Endocrine Disruption

    EPA is required to develop a screening program to determine whether 
certain substances (including all pesticides and inerts) ``may have an 
effect in humans that is similar to an effect produced by a naturally 
occurring estrogen, or such other endocrine effect...'' The Agency is 
currently working with interested stakeholders, including other 
government agencies, public interest groups, industry and research 
scientists in developing a screening and testing program and a priority 
setting scheme to implement this program. Congress has allowed 3 years 
from the passage of FQPA (August 3, 1999) to implement this program. At 
that time, EPA may require further testing of this active ingredient 
and end use products for endocrine disrupter effects.

III. Other Considerations

A. Metabolism In Plants and Animals

     EPA has reviewed the results of plant metabolism studies (apples, 
cabbage, cotton, tomatoes, turnips) and livestock metabolism studies 
(goat and hen). The metabolism of spinosad in plants and animals is 
adequately understood for the purposes of these tolerances. Based on 
structure/activity relationships, EPA concluded that the spinosad 
metabolites/fermentation impurities (spinosyns Factor B, Factor B or D, 
Factor K, and other related Factors) were of no more toxicological 
concern than the two parent compounds (spinosyns Factor A and Factor 
D).
    EPA focused on the following data/information: the overall low 
toxicity of

[[Page 43636]]

spinosad; the low levels of metabolites/fermentation impurities 
present; and that spinosad appears to photodegrade rapidly and become 
incorporated into the general carbon pool. EPA concluded that only 2 
parent compounds (spinosyns Factor A and Factor D) need to be included 
in the tolerance expression and used for dietary risk assessment 
purposes.

B. Analytical Enforcement Methodology

     Method GRM 94.02 (method for determination of spinosad residues in 
cottonseed and related commodities using HPLC/UV) underwent successful 
independent lab validation and EPA lab validation and has been 
submitted to FDA for inclusion in PAM II as Method I. Additional 
methods have been submitted for other crop matrices (leafy vegetables - 
GRM 95.17; citrus - GRM 96.09; tree nuts - GRM 96.14; fruiting 
vegetables - GRM 95.04; and cotton gin byproducts - GRM 94.02.S1). All 
of these methods are essentially similar to GRM 94.02 and have been 
submitted to FDA for inclusion in PAM II as letter methods. These 
methods are adequate for regulation of the tolerance expression.
    Method RES 94094 (method for determination of spinosad residues in 
ruminant commodities using HPLC/UV) underwent successful independent 
lab validation and EPA lab validation and has been submitted to FDA for 
inclusion in PAM II as Method I. This method is adequate for regulation 
of the tolerance expression.
    Method RES 95114 (method for determination of spinosad residues in 
ruminant commodities using immunoassay) underwent successful 
independent lab validation and EPA lab validation and has been 
submitted to FDA for inclusion in PAM II as Method I. This method is 
adequate for regulation of the tolerance expression.

C. International Residue Limits

    No CODEX, Canadian, or Mexican MRLs have been established for 
residues of spinosad on any crops.

IV. Conclusion

    Therefore, a time-limited tolerance is established for residues of 
spinosad in coffee at 0.02 ppm.

V. Objections and Hearing Requests

    The new FFDCA section 408(g) provides essentially the same process 
for persons to ``object'' to a tolerance regulation issued by EPA under 
new section 408(e) and (l)(6) as was provided in the old section 408 
and in section 409. However, the period for filing objections is 60 
days, rather than 30 days. EPA currently has procedural regulations 
which govern the submission of objections and hearing requests. These 
regulations will require some modification to reflect the new law. 
However, until those modifications can be made, EPA will continue to 
use those procedural regulations with appropriate adjustments to 
reflect the new law.
    Any person may, by Ocotber 13, 1998, file written objections to any 
aspect of this regulation and may also request a hearing on those 
objections. Objections and hearing requests must be filed with the 
Hearing Clerk, at the address given above (40 CFR 178.20). A copy of 
the objections and/or hearing requests filed with the Hearing Clerk 
should be submitted to the OPP docket for this rulemaking. The 
objections submitted must specify the provisions of the regulation 
deemed objectionable and the grounds for the objections (40 CFR 
178.25). Each objection must be accompanied by the fee prescribed by 40 
CFR 180.33(i). If a hearing is requested, the objections must include a 
statement of the factual issues on which a hearing is requested, the 
requestor's contentions on such issues, and a summary of any evidence 
relied upon by the requestor (40 CFR 178.27). A request for a hearing 
will be granted if the Administrator determines that the material 
submitted shows the following: There is genuine and substantial issue 
of fact; there is a reasonable possibility that available evidence 
identified by the requestor would, if established, resolve one or more 
of such issues in favor of the requestor, taking into account 
uncontested claims or facts to the contrary; and resolution of the 
factual issues in the manner sought by the requestor would be adequate 
to justify the action requested (40 CFR 178.32). Information submitted 
in connection with an objection or hearing request may be claimed 
confidential by marking any part or all of that information as 
Confidential Business Information (CBI). Information so marked will not 
be disclosed except in accordance with procedures set forth in 40 CFR 
part 2. A copy of the information that does not contain CBI must be 
submitted for inclusion in the public record. Information not marked 
confidential may be disclosed publicly by EPA without prior notice.

VI. Public Record and Electronic Submissions

    EPA has established a record for this rulemaking under docket 
control number [OPP-300693A] (including any comments and data submitted 
electronically). A public version of this record, including printed, 
paper versions of electronic comments, which does not include any 
information claimed as CBI, is available for inspection from 8:30 a.m. 
to 4 p.m., Monday through Friday, excluding legal holidays. The public 
record is located in Room 119 of the Public Information and Records 
Integrity Branch, Information Resources and Services Division (7502C), 
Office of Pesticide Programs, Environmental Protection Agency, Crystal 
Mall #2, 1921 Jefferson Davis Highway, Arlington, VA.
    Electronic comments may be sent directly to EPA at:
    [email protected].


    Electronic comments must be submitted as an ASCII file avoiding the 
use of special characters and any form of encryption.
    The official record for this rulemaking, as well as the public 
version, as described above will be kept in paper form. Accordingly, 
EPA will transfer any copies of objections and hearing requests 
received electronically into printed, paper form as they are received 
and will place the paper copies in the official rulemaking record which 
will also include all comments submitted directly in writing. The 
official rulemaking record is the paper record maintained at the 
Virginia address in ``ADDRESSES'' at the beginning of this document.

VII. Regulatory Assessment Requirements

    This final rule establishes a time-limited tolerance 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). 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., or 
impose any enforceable duty or contain any unfunded mandate as 
described under Title II of the Unfunded Mandates Reform Act of 1995 
(UMRA) (Pub. L. 104-4). Nor does it require any prior consultation as 
specified by Executive Order 12875, entitled Enhancing the 
Intergovernmental Partnership (58 FR 58093, October 28, 1993), or 
special considerations as required by Executive Order 12898, entitled 
Federal Actions to Address Environmental Justice in Minority 
Populations and Low-Income Populations (59 FR 7629, February 16, 1994), 
or require OMB review in

[[Page 43637]]

accordance with Executive Order 13045, entitled Protection of Children 
from Environmental Health Risks and Safety Risks (62 FR 19885, April 
23, 1997).
    In addition, since these tolerances and exemptions that are 
established on the basis of a petition under FFDCA section 408(d), such 
as the [time-limited 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. 
Nevertheless, the Agency has previously assessed whether establishing 
tolerances, exemptions from tolerances, raising tolerance levels or 
expanding exemptions might adversely impact small entities and 
concluded, as a generic matter, that there is no adverse economic 
impact. The factual basis for the Agency's generic certification for 
tolerance actions published on May 4, 1981 (46 FR 24950) and was 
provided to the Chief Counsel for Advocacy of the Small Business 
Administration.

VIII. Submission to Congress and the General Accounting Office

    The Congressional Review Act, 5 U.S.C. 801 et seq., as added by the 
Small Business Regulatory Enforcement Fairness Act of 1996, generally 
provides that before a rule may take effect, the agency promulgating 
the rule must submit a rule report, which includes a copy of the rule, 
to each House of the Congress and to the Comptroller General of the 
United States. 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 rule is not a 
``major rule'' as defined by 5 U.S.C. 804

List of Subjects in 40 CFR Part 180

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


    Dated: August 11, 1998.

James Jones,

Director, Registration Division, Office of Pesticide Programs.
    Therefore, 40 CFR part 180 is amended as follows:

PART 180--[AMENDED]

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

    Authority: 21 U.S.C. 346a and 371.


    2. In Sec. 180.495, paragraph (a) is revised to read as follows:


Sec. 180.495  Spinosad; tolerances for residues.

    (a) General. Tolerances are established for residues of the 
insecticide Spinosad. Factor A is 2-[(6-deoxy-2,3,4-tri-O-methyl-
-L-manno-pyranosyl)oxy]-13-[[5-(dimethylamino)-tetrahydro-6-
methyl-2H-pyran-2-yl]oxy]-9-ethyl-
2,3,3a,5a,5b,6,9,10,11,12,13,14,16a,6b-tetradecahydro-14-methyl-1H-as-
Indaceno[3,2-d]oxacyclododecin-7,15-dione. Factor D is 2-[(6-deoxy-
2,3,4-tri-O-methyl--L-manno-pyranosyl)oxy]-13-[[5-
(dimethylamino)-tetrahydri-6-methyl-2H-pyran-2-yl]oxy]-9-ethyl-
2,3,3a,5a,5b,6,9,10,11,12,13,14,16a,16b-tetradecahydro-4,14-dimethyl-
1H-as-Indaceno[3,2-d]oxacyclododecin-7,15-dione.

                                                                        
------------------------------------------------------------------------
                                                          Expiration/   
             Commodity              Parts per million   Revocation Date 
------------------------------------------------------------------------
Almonds...........................               0.02               None
Almond hulls......................                2.0               None
Apples............................                0.2               None
Apple pomace, wet.................                0.5               None
Brassica (cole), leafy vegetables,                                      
 greens subgroup..................               10.0               None
Brassica (cole), leafy vegetables,                                      
 head and stem subgroup...........                2.0               None
Cattle, fat.......................                0.6               None
Cattle, meat......................               0.04               None
Cattle, meat byproducts...........                0.2               None
Citrus fruits group...............                0.3               None
Citrus oil........................                3.0               None
Citrus pulp, dried................                0.5               None
Coffee............................               0.02            8/28/00
Cotton gin byproducts.............                1.5               None
Cottonseed........................               0.02               None
Fruiting vegetables (except                                             
 cucurbits) group.................                0.4               None
Goat, fat.........................                0.6               None
Goat, meat........................               0.04               None
Goat, meat byproducts.............                0.2               None
Hogs, fat.........................                0.6               None
Hogs, meat........................               0.04               None
Hogs, meat byproducts.............                0.2               None
Horses, fat.......................                0.6               None
Horses, meat......................               0.04               None
Horses, meat byproducts...........                0.2               None
Leafy vegetables (except Brassica                                       
 vegetables) group................                8.0               None
Milk, fat.........................                0.5               None
Milk, whole.......................               0.04               None
Sheep, fat........................                0.6               None
Sheep, meat.......................               0.04               None
Sheep, meat byproducts............                0.2               None
------------------------------------------------------------------------

* * * * *
FR Doc. 98-21893 Filed 8-13-98; 8:45 am
BILLING CODE 6560-50-F