[Federal Register Volume 64, Number 67 (Thursday, April 8, 1999)]
[Notices]
[Pages 17171-17179]
From the Federal Register Online via the Government Publishing Office [www.gpo.gov]
[FR Doc No: 99-8775]


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ENVIRONMENTAL PROTECTION AGENCY

[PF-869; FRL-6071-2]


Notice of Filing of Pesticide Petitions

AGENCY: Environmental Protection Agency (EPA).

ACTION: Notice.

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SUMMARY: This notice announces the initial filing of pesticide 
petitions proposing the establishment of regulations for residues of 
certain pesticide chemicals in or on various food commodities.

DATES: Comments, identified by the docket control number PF-869, must 
be received on or before May 10, 1999.

ADDRESSES: By mail submit written comments to: Public Information and 
Records Integrity Branch, Information Resources and Services Division 
(7502C), Office of Pesticides 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.
    Comments and data may also be submitted electronically to: opp-
[email protected]. Follow the instructions under ``SUPPLEMENTARY 
INFORMATION.'' No confidential business information should be submitted 
through e-mail.
    Information submitted as a comment concerning this document may be 
claimed confidential by marking any part or all of that information as 
``Confidential Business Information'' (CBI). CBI should not be 
submitted through e-mail. Information marked as CBI will not be 
disclosed except in accordance with procedures set forth in 40 CFR part 
2. A copy of the comment 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. All written 
comments will be available for public inspection in Rm. 119 at the 
address given above, from 8:30 a.m. to 4 p.m., Monday through Friday, 
excluding legal holidays.

FOR FURTHER INFORMATION CONTACT: The product manager listed in the 
table below:

------------------------------------------------------------------------
                                   Office location/
        Product Manager            telephone number          Address
------------------------------------------------------------------------
Sidney Jackson................  Rm. 272, CM #2, 703-    1921 Jefferson
                                 305-7610, e-            Davis Hwy,
                                 mail:jackson.sidney@e   Arlington, VA
                                 pamail.epa.gov.
Lisa D. Jones.................  Rm. 259, CM #2, 703-    Do.
                                 308-9424, e-
                                 mail:jones.lisa@epama
il.epa.gov. #
------------------------------------------------------------------------

SUPPLEMENTARY INFORMATION: EPA has received pesticide petitions as 
follows proposing the establishment and/or amendment of regulations for 
residues of certain pesticide chemicals in or on various food 
commodities under section 408 of the Federal Food, Drug, and Comestic 
Act (FFDCA), 21 U.S.C. 346a. EPA has determined that these petitions 
contain data or information regarding the elements set forth in section 
408(d)(2); however, EPA has not fully evaluated the sufficiency of the 
submitted data at this time or whether the data support granting of the 
petition. Additional data may be needed before EPA rules on the 
petition.
    The official record for this notice of filing, as well as the 
public version, has been established for this notice of filing under 
docket control number [PF-869] (including comments and data submitted 
electronically as described below). 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 official record is located at the address in 
``ADDRESSES'' at the beginning of this document.
    Electronic comments can 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. Comments and data 
will also be accepted on disks in Wordperfect 5.1 file format or ASCII 
file format. All comments and data in electronic form must be 
identified by the docket number (insert docket number) and appropriate 
petition number. Electronic comments on notice may be filed online at 
many Federal Depository Libraries.

List of Subjects

    Environmental protection, Agricultural commodities, Food additives, 
Feed additives, Pesticides and pests, Reporting and recordkeeping 
requirements.

    Dated: April 2, 1999.


onald R. Stubbs, Acting

Director, Registration Division, Office of Pesticide Programs.

Summaries of Petitions

    Petitioner summaries of the pesticide petitions are printed below 
as required by section 408(d)(3) of the FFDCA. The summaries of the 
petitions were prepared by the petitioners and represent the views of 
the petitioners. EPA is publishing the petition summaries verbatim 
without editing them in any way. The petition summary announces the 
availability of a description of the analytical methods

[[Page 17172]]

available to EPA for the detection and measurement of the pesticide 
chemical residues or an explanation of why no such method is needed.

1. Interregional Research Project No. 4 (IR-4)

PP 6E4766, 7E4898, 7E4899

    EPA has received pesticide petitions [6E4766, 7E4898, 7E4899] from 
the Interregional Research Project Number 4 (IR-4) New Jersey 
Agricultural Experiment Station, P.O. Box 231, Rutgers University, New 
Brunswick, NJ 08903 proposing, pursuant to section 408(d) of the 
Federal Food, Drug, and Cosmetic Act (FFDCA), 21 U.S.C. 346a(d), to 
amend 40 CFR part 180 by establishing tolerances for residues of the 
insecticide imidacloprid [1-[(6-chloro-3-pyridinyl)methyl]-N-nitro-2-
imidazolidinimine and its metabolites containing the 6-chloropyridinyl 
moiety, all expressed as 1-[(6-chloro-3-pyridinyl)methyl]-N-nitro-2-
imidazolidinimine, in or on the raw agricultural commodities (RAC):
    1. PP 6E4766 proposes the establishment of a tolerance for 
cucurbits vegetables (Crop Group 9) at 0.5 parts per million (ppm).
    2. PP 7E4898 proposes the establishment of a tolerance for tuberous 
and corm vegetables at 0.3 ppm and dasheen (taro) at 3.5 ppm.
    3. PP 7E4899 proposes the establishment of a tolerance for 
watercress, upland at 3.5 ppm.
    EPA has determined that the petitions contain data or information 
regarding the elements set forth in section 408(d)(2) of the FFDCA; 
however, EPA has not fully evaluated the sufficiency of the submitted 
data at this time or whether the data support granting of these 
petitions. Additional data may be needed before EPA rules on these 
petitions. Imidacloprid is produced by the Bayer Corporation (Bayer), 
the registrant.

A. Residue Chemistry

    1. Plant and animal metabolism. The nature of the imidacloprid 
residue in plants and livestock is adequately understood. The residues 
of concern are combined residues of imidacloprid and it metabolites 
containing the 6-chloropyridinyl moiety, all calculated as 
imidacloprid.
    2. Analytical method. The analytical method is a common moiety 
method for imidacloprid and its metabolites containing the 6-
chloropyridinyl moiety using a permanganate oxidation, silyl 
derivatization, and capillary gas chromatography mass spectrometry (GC/
MS) selective monitoring. This method has successfully passed a 
petition method validation in EPA labs. There is a confirmatory method 
specifically for imidacloprid and several metabolites utilizing GC/MS 
and high performance liquid chromotography using ultra-violet detection 
(HPLC-UV) which has been validated by the EPA as well. Imidacloprid and 
its metabolites are stable for at least 24 months in the commodities 
when frozen.
    3. Magnitude of residues. For cucurbits, IR-4 performed 6 trials on 
cucumber, 6 trials on summer squash, and 6 trials on cantaloupe spread 
over two growing seasons (1992 and 1993). Trials conducted during the 
1992 growing season used the following use pattern: i) a plant drench 
plus foliar applications, ii) a plant drench, iii) an in-furrow, and 
iv) a sidedress application. In 1993, IR-4 performed work on only the 
plant drench plus foliar treatment use pattern with a zero day pre-
harvest interval (PHI).
    The use pattern with the highest residue levels was the plant 
drench plus foliar application with a zero day. The maximum residues 
observed were 0.39 ppm for melon, 0.34 ppm for cucumber, and 0.28 ppm 
for summer squash. These maximum levels are all very similar and 
support the crop group concept and proposed 0.5 ppm proposed tolerance 
for imidacloprid on cucurbit vegetables.
    Bayer believes that the data used to support the establishment of 
the imidacloprid 3.5 ppm leafy greens tolerance can be used to extend 
the tolerance to cover upland watercress. This is based on the 
similarities of upland watercress to upland cress and garden cress 
(members of crop subgroup 4A). The use patterns and restrictions for 
use on upland watercress would be the same as currently registered for 
garden cress and upland cress.
    Even at exaggerated rates, imidacloprid residues in the potato 
tubers were only 0.25 ppm. Therefore, IR-4 contends that a crop 
subgroup tolerance for tuberous and corm vegetables to include dasheen 
(taro) is justified and appropriate, and no additional crop-specific 
data are required.
    Although Dasheen (taro) leaves are seldom consumed, they are 
occasionally harvested from dasheen (taro) plantings grown primarily 
for the corms. In support of the proposed tolerance on dasheen (taro) 
leaves, IR-4 has noted that a tolerance of 3.5 ppm has been established 
on lettuce under pesticide petition (PP) 3F4231. IR-4 is requesting 
that the EPA use the data presented in PP 3F4231 to establish a 
tolerance for dasheen (taro) leaves. The proposed use pattern on taro 
does not include any foliar applications of imidacloprid. Therefore, it 
is unlikely that imidacloprid residues in or on taro leaves would 
exceed the proposed 3.5 ppm tolerance.

B. Toxicological Profile

    1. Acute toxicity. The acute oral lethal dose (LD)50 
values for imidacloprid technical ranged from 424-475 milligram/
kilogram body weight (mg/kg bwt) in the rat. The acute dermal 
LD50 was greater than 5,000 mg/kg in rats. The 4-hour rat 
inhalation lethal concentration (LC)50 was > 69 mg/cubic 
meters (m 3) air (aerosol). Imidacloprid was not irritating to rabbit 
skin or eyes. Imidacloprid did not cause skin sensitization in guinea 
pigs.
    2. Genotoxicty. Extensive mutagenicity studies conducted to 
investigate point and gene mutations, DNA damage and chromosomal 
aberration, both using in vitro and in vivo test systems show 
imidacloprid to be non-genotoxic.
    3. Reproductive and developmental toxicity. A 2-generation rat 
reproduction study gave a no-observed adverse effect level (NOAEL) of 
100 ppm (8 mg/kg bwt). Rat and rabbit developmental toxicity studies 
were negative at doses up to 30 mg/kg bwt and 24 mg/kg bwt, 
respectively.
    4. Subchronic toxicity. 90-day feeding studies were conducted in 
rats and dogs. The NOAEL's for these tests were 14 mg/kg bwt/day (150 
parts per million (ppm)) and 5 mg/kg bwt/day (200 ppm) for the rat and 
dog studies, respectively.
    5. Chronic toxicity/carcinogenicity. A 2-year rat feeding/
carcinogenicity study was negative for carcinogenic effects under the 
conditions of the study and had a NOAEL of 100 ppm (5.7 mg/kg/ bwt in 
male and 7.6 mg/kg bwt female) for noncarcinogenic effects that 
included decreased body weight gain in females at 300 ppm and increased 
thyroid lesions in males at 300 ppm and females at 900 ppm. A 1-year 
dog feeding study indicated a NOAEL of 1,250 ppm (41 mg/kg bwt). A 2-
year mouse carcinogenicity study that was negative for carcinogenic 
effects under conditions of the study and had a NOAEL of 1,000 ppm (208 
mg/kg/day).
    Imidacloprid has been classified under ``Group E'' (no evidence of 
carcinogenicity) by EPA's reference dose (RfD) committee. There is no 
cancer risk associated with exposure to this chemical. The RfD based on 
the 2-year rat feeding/carcinogenic study with a NOAEL of 5.7 mg/kg bwt 
and 100-fold uncertainty factor, is calculated to be 0.057 mg/kg bwt.
    6. Endocrine disruption. The toxicology database for imidacloprid 
is

[[Page 17173]]

current and complete. Studies in this database include evaluation of 
the potential effects on reproduction and development, and an 
evaluation of the pathology of the endocrine organs following short- or 
long-term exposure. These studies revealed no primary endocrine effects 
due to imidacloprid.

C. Aggregate Exposure

    Imidacloprid is a broad-spectrum insecticide with excellent 
systemic and contact toxicity characteristics with both food and non-
food uses. Imidacloprid is currently registered for use on various food 
crops, tobacco, turf, ornamentals, buildings for termite control, and 
cats and dogs for flea control. Those potential exposures are addressed 
below:
    1. Dietary exposure. For purposes of assessing the potential acute 
and chronic dietary exposure, the registrant, Bayer, has estimated 
exposure based on the Theoretical Maximum Residue Contribution (TMRC). 
The TMRC is obtained by using a model which multiplies the tolerance 
level residue for each commodity by consumption data. The consumption 
data, based on the National Food Consumption Survey (NFCS) 1989-92 data 
base, estimates the amount of each commodity and products derived from 
the commodities that are eaten by the U.S. population and various 
population subgroups.
    i. Acute. For acute dietary exposure the model calculates a margin 
of exposure (MOE) by dividing the estimated human exposure into the 
NOAEL from the appropriate animal study. Commonly, EPA finds MOEs lower 
than 100 to be unacceptable. The EPA has determined that a NOAEL of 24 
mg/kg/day from a developmental toxicity study in rabbits should be used 
to assess acute toxicity and the risk assessment should evaluate acute 
exposure to females 13 years.
    The MOE for imidacloprid derived from previously established 
tolerances, including time limited tolerances, plus the use on dasheen 
(taro) proposed by IR-4 would be 628 for the U.S. population (48 
States), 258 for nursing infants, and 929 for females 13+ years at the 
99 percentile. These MOEs do not exceed the EPA's level of concern for 
acute dietary exposure.
    ii. Chronic. The EPA has determined that the RfD based on the 2-
year rat feeding/carcinogenic study with a NOAEL of 5.7 mg/kg bwt and 
100-fold uncertainty factor, is calculated to be 0.057 mg/kg bwt. As 
published in the Federal Registers of December 13, 1995 (60 FR 64006), 
and June 12, 1996 (61 FR 2674) (petition to establish tolerances on 
leafy green vegetables (PP 5F4522/R2237)), the TMRC from published uses 
is 0.008358 mg/kg bwt/day which utilizes 14.7% of the RfD for the 
general population. For the most highly exposed subgroup in the 
population, non-nursing infants (< 1 year old), the TMRC for the 
published tolerances is 0.01547 mg/kg/day, which utilizes 27.1% of the 
RfD. Using these conservative assumptions, Bayer has determined that 
the TMRC from published and proposed uses is 0.008498 mg/kg bwt/day 
(15% of the RfD) for the general population and 0.015684 mg/kg/day 
(27.5% of the RfD) for the most highly exposed subgroup in the 
population, non-nursing infants (< 1 year old). Therefore, Bayer 
concludes that dietary exposure from the existing uses and proposed 
uses on cucurbits will not exceed the reference dose for any 
subpopulation (including infants and children).
    iii. Drinking water. The EPA has determined that imidacloprid is 
persistent and could potentially leach into groundwater. However, there 
is no established Maximum Contamination Level (MCL) or health advisory 
levels established for imidacloprid in drinking water. EPA's 
``Pesticides in Groundwater Database'' has no entry for imidacloprid. 
In addition, Bayer is not aware of imidacloprid being detected in any 
wells, ponds, lakes, streams, etc. from its use in the U.S. In studies 
conducted in 1995, imidacloprid was not detected in 17 wells on potato 
farms in Quebec, Canada. Therefore, Bayer concludes that contributions 
to the dietary burden from residues of imidacloprid in water would be 
inconsequential.
    2. Non-dietary exposure--i. Residential Turf. Bayer has conducted 
an exposure study to address the potential exposures of adults and 
children from contact with imidacloprid treated turf. The population 
considered to have the greatest potential exposure from contact with 
pesticide treated turf soon after pesticides are applied are young 
children. Margins of safety (MOS) of 7,587 - 41,546 for 10-year old 
children and 6,859 - 45,249 for 5-year old children were estimated by 
comparing dermal exposure doses to the imidacloprid NOAEL of 1,000 mg/
kg/day established in a 15-day dermal toxicity study in rabbits. The 
estimated safe residue levels of imidacloprid on treated turf for 10-
year old children ranged from 5.6 - 38.2 g/cm2 and 
for 5-year old children from 5.1 - 33.5 g/cm2. This 
compares with the average imidacloprid transferable residue level of 
0.080 g/cm2 present immediately after the sprays 
have dried. These data indicate that children can safely contact 
imidacloprid-treated turf as soon after application as the spray has 
dried.
    ii. Termiticide-- Imidacloprid is registered as a termiticide. Due 
to the nature of the treatment for termites, exposure would be limited 
to that from inhalation and was evaluated by Bayer. Data indicate that 
the MOS for the worst case exposures for adults and infants occupying a 
treated building who are exposed continuously (24 hours/day) are 8.0 x 
107 and 2.4 x 108, respectively - and exposure 
can thus be considered negligible.
    iii. Tobacco smoke. Studies have been conducted to determine 
residues in tobacco and the resulting smoke following treatment. 
Residues of imidacloprid in cured tobacco following treatment were a 
maximum of 31 ppm (7 ppm in fresh leaves). When this tobacco was burned 
in a pyrolysis study only 2% of the initial residue was recovered in 
the resulting smoke (main stream plus side stream). This would result 
in an inhalation exposure to imidacloprid from smoking of approximately 
0.0005 mg per cigarette. Using the measured subacute rat inhalation 
NOAEL of 5.5 mg/m3, Bayer believes that exposure to 
imidacloprid from smoking (direct and/or indirect exposure) would not 
be significant.
    iv. Pet treatment. Bayer concludes that human exposure from the use 
of imidacloprid to treat dogs and cats for fleas does not pose 
unacceptable risks to human health since imidacloprid is not an 
inhalation or dermal toxicant and that while dermal absorption data are 
not available, imidacloprid is not considered to present a hazard via 
the dermal route.

D. Cumulative Effects

    No other chemicals having the same mechanism of toxicity are 
currently registered, therefore, Bayer concludes that there is no risk 
from cumulative effects from other substances with a common mechanism 
of toxicity.

E. Safety Determination

    1. U.S. population--U.S. population in general. Using the 
conservative exposure assumptions described above and based on the 
completeness and reliability of the toxicity data, Bayer concludes that 
total aggregate exposure to imidacloprid from all current uses 
including those currently proposed will utilize little more than 15% of 
the RfD for the U.S. population. EPA generally has no concerns for 
exposures below 100% of the RfD, because the RfD represents the level 
at or below which daily aggregate exposure over a lifetime will not 
pose appreciable risks to human health. Thus, it can be

[[Page 17174]]

concluded that there is a reasonable certainty that no harm will result 
from aggregate exposure to imidacloprid residues.
    2. Infants and children. In assessing the potential for additional 
sensitivity of infants and children to residues of imidacloprid, the 
data from developmental studies in both rat and rabbit and a 2-
generation reproduction study in the rat have been considered. The 
developmental toxicity studies evaluate potential adverse effects on 
the developing animal resulting from pesticide exposure of the mother 
during prenatal development. The reproduction study evaluates effects 
from exposure to the pesticide on the reproductive capability of mating 
animals through 2-generations, as well as any observed systemic 
toxicity.
    FFDCA Section 408 provides that EPA may apply an additional safety 
factor for infants and children in the case of threshold effects to 
account for pre- and post- natal effects and the completeness of the 
toxicity database. Based on current toxicological data requirements, 
the toxicology database for imidacloprid relative to pre- and post-
natal effects is complete. Further for imidacloprid, the NOAEL of 5.7 
mg/kg bwt from the 2-year rat feeding/carcinogenic study, which was 
used to calculate the RfD (discussed above), is already lower than the 
NOAELs from the developmental studies in rats and rabbits by a factor 
of 4.2 to 17.5 times. Since a 100-fold uncertainty factor is already 
used to calculate the RfD, Bayer surmises that an additional 
uncertainty factor is not warranted and that the RfD at 0.057 mg/kg 
bwt/day is appropriate for assessing aggregate risk to infants and 
children.
    Using the conservative exposure assumptions described above under 
aggregate exposure, Bayer has determined from a chronic dietary 
analysis that the percent of the RfD utilized by aggregate exposure to 
residues of imidacloprid ranges from 9.3% for nursing infants up to 
32.2% for children (1-6 years). EPA generally has no concern for 
exposure below 100% of the RfD. In addition, the MOEs for all infant 
and children population groups do not exceed EPA's level of concern for 
acute dietary exposure. Therefore, based on the completeness and 
reliability of the toxicity data and the conservative exposure 
assessment, Bayer concludes that there is a reasonable certainty that 
no harm will result to infants and children from aggregate exposure to 
the residues of imidacloprid, including all anticipated dietary 
exposure and all other non-occupational exposures.

F. International Tolerances

    No CODEX Maximum Residue Levels (MRLs) have been established for 
residues of imidacloprid on any crops at this time.

2. IR-4 Project

 PP 8E5034

    EPA has received a pesticide petition (8E5034) from the 
Interregional Research Project Number 4 (IR-4), proposing pursuant to 
section 408(d) of the Federal Food, Drug, and Cosmetic Act, 21 U.S.C. 
346a(d), to amend 40 CFR part 180 by establishing a tolerance for 
residues of the insecticide, spinosad in or on the raw agricultural 
commodities (RAC) tuberous and corm vegetables (crop subgroup 1C) at 
0.03 parts per million (ppm). EPA has determined that the petition 
contains data or information regarding the elements set forth in 
section 408(d)(2) of the FFDCA; however, EPA has not fully evaluated 
the sufficiency of the submitted data at this time or whether the data 
support granting of the petition. Additional data may be needed before 
EPA rules on the petition. Spinosad is produced by Dow AgroSciences, 
Inc. (Dow), the registrant,

A. Residue Chemistry

    1. Plant metabolism. The metabolism of spinosad in plants (apples, 
cabbage, cotton, tomato, and turnip), and animals (goats and poultry) 
is adequately understood for the purposes of this tolerance. A 
rotational crop study showed no carryover of measurable spinosad 
related residues in representative test crops.
    2. Analytical method. There is a practical method (immunoassay) for 
detecting (0.005 ppm) and measuring (0.01 ppm) levels of spinosad in or 
on food with a limit of detection that allows monitoring of food with 
residues at or above the level set for this tolerance. The method has 
had a successful method tryout in the EPA's laboratories.
    3. Magnitude of residues. Magnitude of residue studies were 
conducted for potatoes at 14 sites. No quantifiable residues were 
observed in treated field samples at an application rate of 0.11 pounds 
active ingredient (lb a.i.) per acre or at an exaggerated application 
rate of 0.55 lb a.i. per acre. A potato processing study is not 
required because there were no quantifiable residues in the RAC even at 
the 5x application rate (5x is the maximum theoretical concentration 
factor for potato). Potato is the representative crop for the tuberous 
and corm vegetables crop subgroup 1C.

B. Toxicological Profile

    1. Acute toxicity--Spinosad has low acute toxicity. The rat oral 
lethal dose (LD)50 is 3,738 milligram kilogram (mg/kg) for 
males and > 5,000 mg/kg for females, whereas the mouse oral 
LD50 is > 5,000 mg/kg. The rabbit dermal LD50 is 
> 5,000 mg/kg and the rat inhalation lethal concentration 
(LC)50 is > 5.18 mg/liter(l) air. In addition, spinosad is 
not a skin sensitizer in guinea pigs and does not produce significant 
dermal or ocular irritation in rabbits. End use formulations of 
spinosad that are water based suspension concentrates have similar low 
acute toxicity profiles.
    2. Genotoxicty. Short term assays for genotoxicity consisting of a 
bacterial reverse mutation assay (Ames test), an in vitro assay for 
cytogenetic damage using the Chinese hamster ovary cells, an in vitro 
mammalian gene mutation assay using mouse lymphoma cells, an in vitro 
assay for DNA damage and repair in rat hepatocytes, and an in vivo 
cytogenetic assay in the mouse bone marrow (micronucleus test) have 
been conducted with spinosad. These studies show a lack of 
genotoxicity.
    3. Reproductive and developmental toxicity. Spinosad caused 
decreased body weights in maternal rats given 200 mg/kg/day by gavage, 
highest dose tested (HTD). This was not accompanied by either embryo 
toxicity, fetal toxicity, or teratogenicity. The no-observed adverse 
effect levels (NOAELs) for maternal and fetal toxicity in rats were 50 
and 200 mg/kg/day, respectively. A teratology study in rabbits showed 
that spinosad caused decreased body weight gain and a few abortions in 
maternal rabbits given 50 mg/kg/day, HTD. Maternal toxicity was not 
accompanied by either embryo toxicity, fetal toxicity, or 
teratogenicity. The NOAELs for maternal and fetal toxicity in rabbits 
were 10 and 50 mg/kg/day, respectively. In a 2-generation reproduction 
study in rats, parental toxicity was observed in both males and females 
given 100 mg/kg/day HTD. Perinatal effects (decreased litter size and 
pup weight) at 100 mg/kg/day were attributed to maternal toxicity. The 
NOAEL for maternal and pup effects was 10 mg/kg/day.
    4. Subchronic toxicity. Spinosad was evaluated in 13-week dietary 
studies and showed NOAELs of 4.89 and 5.38 mg/kg/day, respectively in 
male and female dogs; 6 and 8 mg/kg/day, respectively in male and 
female mice; and 33.9 and 38.8 mg/kg/day, respectively in male and 
female rats. No dermal irritation or systemic toxicity occurred in a 
21-day repeated dose dermal toxicity study in rabbits given 1,000 mg/
kg/day.

[[Page 17175]]

    5. Chronic toxicity. Based on chronic testing with spinosad in the 
dog and the rat, the EPA has set a reference dose (RfD) of 0.027 mg/kg/
day for spinosad. The RfD has incorporated a 100-fold safety factor to 
the NOAELs found in the chronic dog study to account for inter- and 
intra-species variation. The NOAELs shown in the dog chronic study were 
2.68 and 2.72 mg/kg/day, respectively for male and female dogs. The 
NOAELs (systemic) shown in the rat chronic/carcinogenicity/
neurotoxicity study were 9.5 and 12.0 mg/kg/day, respectively for male 
and female rats. Using the Guidelines for Carcinogen Risk Assessment 
published September 24, 1986 (51 FR 33992), it is proposed that 
spinosad be classified as Group E for carcinogenicity (no evidence of 
carcinogenicity) based on the results of carcinogenicity studies in two 
species. There was no evidence of carcinogenicity in an 18-month mouse 
feeding study and a 24-month rat feeding study at all dosages tested. 
The NOAELs shown in the mouse carcinogenicity study were 11.4 and 13.8 
mg/kg/day, respectively for male and female mice. A maximum tolerated 
dose was achieved at the top dosage level tested in both of these 
studies based on excessive mortality. Thus, the doses tested are 
adequate for identifying a cancer risk. Accordingly, a cancer risk 
assessment is not needed.
    6. Animal metabolism. There were no major differences in the 
bioavailability, routes or rates of excretion, or metabolism of 
spinosyn A and spinosyn D following oral administration in rats. Urine 
and fecal excretions were almost completed in 48-hours post-dosing. In 
addition, the routes and rates of excretion were not affected by 
repeated administration.
    7. Metabolite toxicology. The residue of concern for tolerance 
setting purposes is the parent material (spinosyn A and spinosyn D). 
Thus, there is no need to address metabolite toxicity.
    8. Neurotoxicity. Spinosad did not cause neurotoxicity in rats in 
acute, subchronic or chronic toxicity studies.
    9. Endocrine disruption. There is no evidence to suggest that 
spinosad has an effect on any endocrine system.

C. Aggregate Exposure

    1. Dietary exposure--i. Food. For purposes of assessing the 
potential dietary exposure from use of spinosad on tuberous and corm 
vegetables as well as from other existing and pending spinosad crop 
uses, a conservative estimate of aggregate exposure is determined by 
basing the theoretical maximum residue concentration (TMRC) on the 
proposed tolerance level for spinosad and assuming that 100% of these 
proposed new crops and other pending and existing (registered for use) 
crops grown in the United State were treated with spinosad. The TMRC is 
obtained by multiplying the tolerance residue levels by the consumption 
data which estimates the amount of crops and related food stuffs 
consumed by various population subgroups. The use of a tolerance level 
and 100% of crop treated clearly results in an overestimate of human 
exposure and a safety determination for the use of spinosad on crops 
cited in this summary that is based on a conservative exposure 
assessment.
    ii. Drinking water. Another potential source of dietary exposure 
are residues in drinking water. Based on the available environmental 
studies conducted with spinosad wherein it's properties show little or 
no mobility in soil, Dow concludes that there is no anticipated 
exposure to residues of spinosad in drinking water. In addition, there 
is no established maximum concentration level (MCL) for residues of 
spinosad in drinking water.
    2. Non-dietary exposure. Spinosad is currently registered for use 
on a number of crops including cotton, fruits, and vegetables in the 
agriculture environment. Spinosad is also currently registered for 
outdoor use on turf and ornamentals at low rates of application (0.04 
to 0.54 lb a.i. per acre) and indoor use for drywood termite control 
(extremely low application rates used with no occupant exposure 
expected). Thus, Dow believes that the potential for non-dietary 
exposure to the general population is considered negligible.

D. Cumulative Effects

    The potential for cumulative effects of spinosad and other 
substances that have a common mechanism of toxicity is also considered. 
In terms of insect control, spinosad causes excitation of the insect 
nervous system, leading to involuntary muscle contractions, prostration 
with tremors, and finally paralysis. These effects are consistent with 
the activation of nicotinic acetylcholine receptors by a mechanism that 
is clearly novel and unique among known insecticidal compounds. 
Spinosad also has effects on the gamma aminobatopic acid (GABA) 
receptor function that may contribute further to its insecticidal 
activity. Based on results found in tests with various mammalian 
species, spinosad appears to have a mechanism of toxicity like that of 
many amphiphilic cationic compounds. There is no reliable information 
to indicate that toxic effects produced by spinosad would be cumulative 
with those of any other pesticide chemical. Thus Dow contends that it 
is appropriate to consider only the potential risks of spinosad in an 
aggregate exposure assessment.

E. Safety Determination

    1. U.S. population. Using the conservative exposure assumptions and 
the proposed RfD described above, the aggregate exposure to spinosad 
use on tuberous and corm vegetables and other pending and existing crop 
uses will utilize 25.5% of the RfD for the U.S. population. A more 
realistic estimate of dietary exposure and risk relative to a chronic 
toxicity endpoint is obtained if average (anticipated) residue values 
from field trials are used. Inserting the average residue values in 
place of tolerance residue levels produces a more realistic, but still 
conservative risk assessment. Based on average or anticipated residues 
in a dietary risk analysis, the use of spinosad on tuberous and corm 
vegetables and other pending and existing crop uses will utilize 4.1% 
of the RfD for the U.S. population. 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. Thus, Dow believes that 
there is reasonable certainty that no harm will result from aggregate 
exposure to spinosad residues on existing and pending crop uses.
    2. Infants and children. In assessing the potential for additional 
sensitivity of infants and children to residues of spinosad, data from 
developmental toxicity studies in rats and rabbits and a 2-generation 
reproduction study in the rat are considered. The developmental 
toxicity studies are designed to evaluate adverse effects on the 
developing organism resulting from pesticide exposure during prenatal 
development. Reproduction studies provide information relating to 
effects from exposure to the pesticide on the reproductive capability 
and potential systemic toxicity of mating animals and on various 
parameters associated with the well-being of pups.
    FFDCA Section 408 provides that EPA may apply an additional safety 
factor for infants and children in the case of threshold effects to 
account for pre- and post-natal toxicity and the completeness of the 
database. Based on the current toxicological data requirements, the 
database for spinosad relative to pre- and post-natal effects for 
children is complete. Further, for spinosad, the NOAELs in the dog 
chronic feeding study which was used to calculate the

[[Page 17176]]

RfD (0.027 mg/kg/day) are already lower than the NOAELs from the 
developmental studies in rats and rabbits by a factor of more than 10-
fold.
    Concerning the reproduction study in rats, the pup effects shown at 
the HDT were attributed to maternal toxicity. Therefore, the registrant 
concludes that an additional uncertainty factor is not needed and that 
the RfD at 0.027 mg/kg/day is appropriate for assessing risk to infants 
and children.
    In addition, the EPA has determined that the 10x factor to account 
for enhanced sensitivity of infants and children is not needed 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 
two-generation reproduction 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.
    Using the conservative exposure assumptions previously described 
(tolerance level residues), the percent RfD utilized by the aggregate 
exposure to residues of spinosad on tuberous and corm vegetables and 
other pending and existing crop uses is 51.2% for children 1 to 6 years 
old, the most sensitive population subgroup. If average or anticipated 
residues are used in the dietary risk analysis, the use of spinosad on 
these crops will utilize 9.4% of the RfD for children 1 to 6 years old. 
Thus, based on the completeness and reliability of the toxicity data 
and the conservative exposure assessment, the registrant concludes that 
there is reasonable certainty that no harm will result to infants and 
children from aggregate exposure to spinosad residues on the above 
proposed use including other pending and existing crop uses.

F. International Tolerances

    There are no Codex maximum residue levels established for residues 
of spinosad on tuberous and corm vegetables or any other food or feed 
crop.

3. Zeneca Ag. Products

 PP 7F4854, 7F4876, and 7F4853

    EPA has received pesticide petitions [7F4854, 7F876, and 7F4853] 
from Zeneca Ag.Products, 1800 Concord Pike, P. O. Box 15458, 
Wilmington, DE 19850-5458 proposing, pursuant to section 408(d) of the 
Federal Food, Drug, and Cosmetic Act (FFDCA), 21 U.S.C. 346a(d), to 
amend 40 CFR part 180 by establishing a tolerance for residues of 
sulfosate (the trimethylsulfonium salt of glyphosate, also known as 
glyphosate-trimesium in or on the raw agricultural commodity (RAC) the 
fruiting vegetables (except cucurbits) group at 0.05 ppm; the edible-
podded legume vegetables subgroup at 0.5 ppm (of which no more than 0.3 
ppm is trimethylsulfonium (TMS)), the succulent shelled pea and bean 
subgroup at 0.2 ppm (of which no more than 0.1 ppm is TMS); the dried 
shelled pea and bean (except soybean) subgroup at 6 ppm (of which no 
more than 1.5 ppm is TMS); in cattle, goat, hog, sheep, and horse 
kidney at 3.5 ppm; in cattle, goat, hog, sheep, and horse meat by-
products, except liver and kidney, at 2.5 ppm; and to increase the 
tolerance in cattle, goat, hog, sheep, and horse fat to 0.2 ppm; in 
cattle, goat, hog, sheep, and horse meat to 0.6 ppm; in cattle, goat, 
hog, sheep, and horse liver to 0.75 ppm; in milk to 1.1 ppm; in poultry 
liver to 0.1 ppm; in poultry meat by-products to 0.25 ppm; in or on 
soybean seed to 21 ppm (of which no more than 13 ppm is TMS); in 
soybean hulls to 45 ppm (of which no more than 25 ppm is TMS); and in 
aspirated grain fractions to 1,300 ppm (of which no more than 720 ppm 
is TMS) at parts per million (ppm). EPA has determined that the 
petition contains data or information regarding the elements set forth 
in section 408(d)(2) of the FFDCA; however, EPA has not fully evaluated 
the sufficiency of the submitted data at this time or whether the data 
supports granting of the petition. Additional data may be needed before 
EPA rules on the petition.

A. Residue Chemistry

    1. Plant metabolism. The metabolism of sulfosate has been studied 
in corn, grapes, and soybeans. EPA has concluded that the nature of the 
residue is adequately understood and that the only residues of concern 
are the parent ionsN-(phosphonomethyl)-glycine anion (PMG) and 
trimethylsulfonium cation (TMS).
    2. Analytical method. Gas chromatography/mass selective (GC/MS) 
detector methods have been developed for PMG analysis in crops, animal 
tissues, milk, and eggs. Gas chromatography detection methods have been 
developed for TMS in crops, animal tissues, milk, and eggs.
    3. Magnitude of residues--i. Magnitude of residues in crops-- 
Soybeans. Residue data are available for sulfosate in a total of 20 
trials conducted in 3 different EPA regions and 15 different States 
representing 99% of the soybean production in the U.S. The proposed 
tolerance of 21 ppm (of which no more than 13 ppm is TMS) for soybean 
seed will accommodate any residue resulting from the proposed use 
pattern.
    Soybean seed for processing were obtained and samples were 
processed into hulls, meal, crude oil, refined oil, and soapstock. 
Aspirated grain fractions were also collected. Analysis of the treated 
samples showed that residue of both TMS and PMG accumulated in hulls 
but did not accumulate in any other processed fractions. The proposed 
tolerance of 45 ppm (of which no more than 25 ppm is TMS) for soybean 
hulls and 1,300 ppm (of which no more than 720 ppm is TMS) for 
aspirated grain fractions will accommodate any residue resulting from 
the proposed use pattern.
    ii. Fruiting vegetables (except curcurbits) group. Residue data are 
available for sulfosate in a total of 12 trials in tomatoes conducted 
in 5 EPA regions and 5 different states; a total of 6 trials in bell 
peppers conducted in 5 EPA regions and 6 different States; and a total 
of 3 trials in chili peppers conducted in 3 EPA regions and 3 different 
States. The residue levels were below the limit of quantitation (LOQ) 
of 0.05 ppm in all samples. The proposed tolerance of 0.05 ppm will 
accommodate any residue resulting from the proposed use pattern.
    Tomato fruits for processing were obtained and samples were 
processed into puree and paste. After adjusting the results for the 
exaggerated rate, no concentration occurred in the puree and paste. No 
tolerances are required for puree and paste at the proposed use rates.
    iii. Edible podded legume vegetables subgroup. Residue data are 
available for sulfosate in a total of 9 trials conducted in 5 different 
EPA regions and 8 different States representing 94% of the edible 
podded beans and peas in the U.S. The proposed tolerance of 0.5 ppm (of 
which no more than 0.3 ppm is TMS) for the Edible podded legume 
vegetables subgroup will accommodate any residue resulting from the 
proposed use pattern.
    iv. Succulent shelled pea and bean subgroup. Residue data are 
available for sulfosate in a total of 12 trials in 6 different EPA 
regions and 10 different States representing 97% of the green peas and 
lima beans in the United States. The proposed tolerance of 0.2 ppm (of 
which no more than 0.1 ppm is TMS) for the Succulent shelled pea and 
bean subgroup will accommodate any residue resulting from the proposed 
use pattern.

[[Page 17177]]

    v. Dried shelled pea and bean (except soybean) subgroup. Residue 
data are available for sulfosate in a total of 14 trials conducted in 5 
different EPA Regions and in 8 States representing 97% of dried pea and 
96% of dried bean production in the United States. The proposed 
tolerance of 6 ppm (of which no more than 1.5 ppm is TMS) for the Dried 
shelled pea and bean (except soybean) subgroup will accommodate any 
residue resulting from the proposed use pattern.
    vi. Magnitude of residue in animals--Ruminants. The maximum dietary 
burden in dairy cows results from a diet comprised of 20% aspirated 
grain fractions, 60% wheat forage, and 20% wheat hay for a total 
dietary burden of 409 ppm. The maximum dietary burden in beef cows 
results from a diet comprised of 20% aspirated grain fractions, 25% 
wheat forage, 25% wheat hay, 20% soybean hulls, and 10% soybean seed 
for a total dietary burden of 378 ppm. Comparison to a ruminant feeding 
study at a dosing level of 300 ppm indicates that the appropriate 
tolerance levels are 0.75 ppm in cattle, goat, hog, sheep, and horse 
liver; 3.5 ppm in cattle, goat, hog, sheep, and horse kidney; 2.5 ppm 
in cattle, goat, hog, sheep, and horse meat by-products, except kidney 
and liver; 0.6 ppm in cattle, goat, hog, sheep, and horse meat; 1.1 ppm 
in milk; and 0.2 ppm in cattle, goat, hog, sheep, and horse fat. All of 
these tolerances exceed existing tolerances in 40 CFR 180.489.
    vii. Poultry. The maximum dietary burden in poultry results from a 
diet comprised of 40% soybean meal, 20% soybean hulls, 20% soybean 
seed, and 20% wheat milled by-products for a total dietary burden of 24 
ppm. Comparison to a poultry feeding study at a dosing level of 50 ppm 
indicates that the appropriate tolerance levels are below established 
tolerances for poultry meat, fat, and eggs. The appropriate tolerance 
for poultry liver is 0.1 ppm and for poultry meat by-products is 0.25 
ppm.

B. Toxicological Profile

    1. Acute toxicity. Several acute toxicology studies have been 
conducted placing technical grade sulfosate in Toxicity Category III 
and IV.
    2. Genotoxicty. Mutagenicity data includes two Ames tests with 
Salmonella typhimurium; a sex linked recessive lethal test with 
Drosophila melanoga; a forward mutation (mouse lymphoma) test; an in 
vivo bone marrow cytogenetics test in rats; a micronucleus assay in 
mice; an in vitro chromosomal aberration test in Chinese hamster ovary 
cells (CHO) (no aberrations were observed either with or without S9 
activation and there were no increases in sister chromatid exchanges); 
and a morphological transformation test in mice (all negative). A 
chronic feeding/carcinogenicity study was conducted in male and female 
rats fed dose levels of 0, 100, 500 and 1,000 ppm (0, 4.2., 21.2 or 
41.8 mg/kg/day in males and 0, 5.4, 27.0 or 55.7 mg/kg/day in females). 
No carcinogenic effects were observed under the conditions of the 
study. The systemic no-observable effect level (NOAEL) of 1,000 ppm 
(41.1/55.7 mg/kg/day for males and females, respectively) was based on 
decreased body weight gains (considered secondary to reduced food 
consumption) and increased incidences of chronic laryngeal and 
nasopharyngeal inflammation (males). A chronic feeding/carcinogenicity 
study was conducted in male and female mice fed dosage levels of 0, 
100, 1,000 and 8,000 ppm (0, 11.7, 118 or 991 mg/kg/day in males and 0, 
16, 159 or 1,341 mg/kg/day in females). No carcinogenic effects were 
observed under the conditions of the study at dose levels up to and 
including the 8,000 ppm highest dose tested (HDT) which may have been 
excessive. The systemic NOAEL was 1,000 ppm based on decreases in body 
weight and feed consumption (both sexes) and increased incidences of 
duodenal epithelial hyperplasia (females only). Sulfosate is classified 
as a Group E carcinogen based on no evidence of carcinogenicity in rat 
and mouse studies.
    3. Reproductive and developmental toxicity. A developmental 
toxicity study in rats was conducted at doses of 0, 30, 100 and 333 mg/
kg/day. The maternal (systemic) NOAEL was 100 mg/kg/day, based on 
decreased body weight gain and food consumption, and clinical signs 
(salivation, chromorhinorrhea, and lethargy) seen at 333 mg/kg/day. The 
reproductive NOAEL was 100 mg/kg/day, based on decreased mean pup 
weight. The decreased pup weight is a direct result of the maternal 
toxicity. A developmental toxicity study was conducted in rabbits at 
doses of 0, 10, 40 and 100 mg/kg/day with developmental and maternal 
toxicity NOAELs of 40 mg/kg/day based on the following: (1) Maternal 
effects: 6 of 17 dams died (2 of the 4 non-gravid dams); 4 of 11 dams 
aborted; clinical signs - higher incidence and earlier onset of 
diarrhea, anorexia, decreased body weight gain and food consumption; 
and, (2) Fetal effects: decreased litter sizes due to increased post-
implantation loss, seen at 100 mg/kg/day (HDT). The fetal effects were 
clearly a result of significant maternal toxicity. A 2-generation 
reproduction study in rats fed dosage rates of 0, 150, 800 and 2,000 
ppm (equivalent to calculated doses of 0, 7.5, 40, and 100 mg/kg/day 
for males and females, based on a conversion factor of 1 mg/kg-day = 20 
ppm). The maternal (systemic) NOAEL was 150 ppm (7.5 mg/kg/day), based 
on decreases in body weight and body weight gains accompanied by 
decreased food consumption, and reduced absolute and sometimes relative 
organ (thymus, heart, kidney and liver) weights seen at 800 and 2,000 
ppm (40 and 100 mg/kg/day). The reproductive NOAEL was 150 ppm (7.5 mg/
kg/day), based on decreased mean pup weights during lactation (after 
day 7) in the second litters at 800 ppm (40 mg/kg/day) and in all 
litters at 2,000 ppm (100 mg/kg/day), and decreased litter size in the 
F0a and F1b litters at 2,000 ppm (100 mg/kg/day). The statistically 
significant decreases in pup weights at the 800 ppm level were 
borderline biologically significant because at no time were either the 
body weights or body weight gains less than 90% of the control values 
and because the effect was not apparent in all litters. Both the slight 
reductions in litter size at 2,000 ppm and the reductions in pup 
weights at 800 and 2,000 ppm appear to be secondary to the health of 
the dams. There was no evidence of altered intrauterine development, 
increased stillborns, or pup anomalies. The effects are a result of 
feed palatability leading to reduced food consumption and decreases in 
body weight gains in the dams.
    4. Subchronic toxicity. Two sub-chronic 90-day feeding studies with 
dogs and a 1-year feeding study in dogs have been conducted. In the 1-
year study dogs were fed 0, 2, 10 or 50 mg/kg/day. The NOAEL was 
determined to be 10 mg/kg/day based on decreases in lactate 
dehydrogenase (LDH) at 50 mg/kg/day. In the first 90-day study, dogs 
were fed dosage levels of 0, 2, 10 and 50 mg/kg/day. The NOAEL in this 
study was 10 mg/kg/day based on transient salivation, and increased 
frequency and earlier onset of emesis in both sexes at 50 mg/kg/day. A 
second 90-day feeding study with dogs dosed at 0, 10, 25 and 50 mg/kg/
day was conducted to refine the threshold of effects. There was 
evidence of toxicity at the top dose of 50 mg/kg/day with a NOAEL of 25 
mg/kg/day. Adverse effects from oral exposure to sulfosate occur at or 
above 50 mg/kg/day. These effects consist primarily of transient 
salivation, which is regarded as a pharmacological rather than 
toxicological effect, emesis and

[[Page 17178]]

non-biologically significant hematological changes. Exposures at or 
below 25 mg/kg/day have not resulted in significant biological adverse 
effects. In addition, a comparison of data from the 90-day and 1-year 
studies indicates that there is no evidence for increased toxicity with 
time. The overall NOAEL in the dog is 25 mg/kg/day.
    5. Chronic toxicity. A chronic feeding/carcinogenicity study was 
conducted in male and female rats fed dose levels of 0, 100, 500 and 
1,000 ppm (0, 4.2, 21.2 or 41.8 mg/kg/day in males and 0, 5.4, 27.0 or 
55.7 mg/kg day in females). No carcinogenic effects were observed under 
the conditions of the study. The systemic NOAEL of 1,000 ppm (41.1/55.7 
mg/kg/day for males and females, respectively) was based on decreased 
body weight gains (considered secondary to reduced food consumption) 
and increased incidences of chronic laryngeal and nasopharyngeal 
inflammation (males). A chronic feeding/carcinogenicity study was 
conducted in male and female mice fed dosage levels of 0, 100, 1,000 
and 8,000 ppm (0, 11.7, 118 or 991 mg/kg/day in males and 0, 16, 159 or 
1,341 mg/kg/day in females). No carcinogenic effects were observed 
under the conditions of the study at dose levels up to and including 
the 8,000 ppm HDT (highest dose may have been excessive). The systemic 
NOAEL was 1,000 ppm based on decreases in body weight and feed 
consumption (both sexes) and increased incidences of duodenal 
epithelial hyperplasia (females only). Sulfosate is classified as a 
Group E carcinogen based on no evidence of carcinogenicity in rat and 
mouse studies.
    6. Animal metabolism. The metabolism of sulfosate has been studied 
in animals. The residues of concern for sulfosate in meat, milk, and 
eggs are the parent ions PMG and TMS only.
    7. Metabolite toxicology. There are no metabolites of toxicological 
concern. Only the parent ions, PMG and TMS are of toxicological 
concern.
    8. Endocrine disruption. Current data suggest that sulfosate is not 
an endocrine disruptor.

C. Aggregate Exposure

    1. Dietary exposure.--i. Food. For the purposes of assessing the 
potential dietary exposure, Zeneca has utilized the tolerance level for 
all existing and pending tolerances; and the proposed maximum 
permissible levels of 0.05 ppm for the fruiting vegetables (except 
cucurbits) group; 0.5 ppm for the edible-podded legume vegetables 
subgroup; 0.2 ppm for the succulent shelled pea and bean subgroup; 6 
ppm for the dried shelled pea and bean (except soybean) subgroup; 3.5 
ppm for cattle, goat, hog, sheep, and horse kidney; 2.5 ppm for cattle, 
goat, hog, sheep, and horse meat by-products, except liver and kidney; 
0.6 ppm for cattle, goat, hog, sheep, and horse meat; 0.75 ppm for 
cattle, goat, hog, sheep, and horse liver; 1.1 ppm for milk; 0.1 ppm 
for poultry liver; 0.25 ppm for poultry meat by-products; 21 ppm for 
soybean seed; 45 ppm for soybean hulls; 1300 ppm for aspirated grain 
fractions; and 100% crop treated acreage for all commodities. Assuming 
that 100% of foods, meat, eggs, and milk products will contain 
sulfosate residues and those residues will be at the level of the 
tolerance results in an overestimate of human exposure. This is a very 
conservative approach to exposure assessment.
    ii. Chronic exposure. For all existing tolerances and pending 
tolerances; and the proposed maximum permissible levels proposed in 
this notice of filing, the potential exposure for the U.S. population 
is 0.018 mg/kg bwt/day (7.4% of RfD). Potential exposure for children's 
population subgroups range from 0.015 mg/kg bwt/day (6.1% of RfD) for 
nursing infants (<1 year old) to 0.076 mg/kg bwt/day (30.5%) for non-
nursing infants. The chronic dietary risk due to food does not exceed 
the level of concern (100%) Acute exposure. The exposure to the most 
sensitive population subgroup, in this instance non-nursing infants, 
was 23.2% of the acute RfD. The acute dietary risk due to food does not 
exceed the level of concern (100%).
    iii. Drinking water. Results from computer modeling indicate that 
sulfosate in groundwater will not contribute significant residues in 
drinking water as a result of sulfosate use at the recommended maximum 
annual application rate (4.00 lbs. a.i. acre -1). The computer model 
uses conservative numbers, therefore it is unlikely that groundwater 
concentrations would exceed the estimated concentration of 0.00224 
parts per billion (ppb), and sulfosate should not pose a threat to 
ground water.
    The surface water estimates are based on an exposure modeling 
procedure called Generic Expected Environmental Concentration (GENEEC). 
The assumptions of 1 application of 4.00 lbs. a.i. acre -1 resulted in 
calculated estimated maximum concentrations of 64 ppb (acute, based on 
the highest 56-day value) and 43 ppb (chronic, average). GENEEC 
modeling procedures assumed that sulfosate was applied to a 10-hectare 
field that drained into a 1-hectare pond, 2-meters deep with no outlet.
    As a conservative assumption, because sulfosate residues in ground 
water are expected to be insignificant compared to surface water, it 
has been assumed that 100% of drinking water consumed was derived from 
surface water in all drinking water exposure and risk calculations.
    To calculate the maximum acceptable acute and chronic exposures to 
sulfosate in drinking water, the dietary food exposure (acute or 
chronic) was subtracted from the appropriate (acute or chronic) RfD. 
Drinking water levels of concern (DWLOCs) were then calculated using 
the maximum acceptable acute or chronic exposure, default body weights 
(70 kg - adult, 10 kg - child), and drinking water consumption figures 
(2 liters - adult, 1 liter - child).
    The maximum concentration of sulfosate in surface water is 64 ppb. 
The acute DWLOCs for sulfosate in surface water were all greater than 
7,700 ppb. The estimated average concentration of sulfosate in surface 
water is 43 ppb which is much less than the calculated levels of 
concern (> 1,700 ppb) in drinking water as a contribution to chronic 
aggregate exposure. Therefore, for current and proposed uses of 
sulfosate, Zeneca concludes with reasonable certainty that residues of 
sulfosate in drinking water would not result in unacceptable levels of 
aggregate human health risk.
    2. Non-dietary exposure. Sulfosate is currently not registered for 
use on any residential non-food sites. Therefore, residential exposure 
to sulfosate residues will be through dietary exposure only.

D. Cumulative Effects

    There is no information to indicate that toxic effects produced by 
sulfosate are cumulative with those of any other chemical compound.

E. Safety Determination

    1. U.S. population--i. Acute risk. Since there are no residential 
uses for sulfosate, the acute aggregate exposure only includes food and 
water. Using the conservative assumptions of 100% of all crops treated 
and assuming all residues are at the tolerance level for all 
established and proposed tolerances, the aggregate exposure to 
sulfosate will utilize 17.3% of the acute RfD for the U.S. population. 
The estimated peak concentrations of sulfosate in surface and ground 
water are less than DWLOCs for sulfosate in drinking water as a 
contribution to acute aggregate exposure. Residues of sulfosate in 
drinking water do not contribute significantly to the aggregate acute 
human health risk considering the

[[Page 17179]]

present uses and uses proposed in this action.
    ii. Chronic risk. Using the conservative exposure assumptions 
described above, the aggregate exposure to sulfosate from food will 
utilize 7.4% of the chronic RfD for the U.S. population. The estimated 
average concentrations of sulfosate in surface and ground water are 
less than DWLOCs for sulfosate in drinking water as a contribution to 
chronic aggregate exposure. Residues of sulfosate in drinking water do 
not contribute significantly to the aggregate chronic human health risk 
considering the present uses and uses proposed in this action.
    2. Infants and children. The database on sulfosate relative to pre- 
and post-natal toxicity is complete. Because the developmental and 
reproductive effects occurred in the presence of parental (systemic) 
toxicity, these data do not suggest an increased pre- or post-natal 
sensitivity of children and infants to sulfosate exposure. Therefore, 
Zeneca concludes, upon the basis of reliable data, that a 100-fold 
uncertainty factor is adequate to protect the safety of infants and 
children and an additional safety factor is unwarranted.
    i. Acute risk. Using the conservative exposure assumptions 
described above, the aggregate exposure to sulfosate from food will 
utilize 23.2% of the acute RfD for the most highly exposed group, non-
nursing infants. The estimated peak concentrations of sulfosate in 
surface and ground water are less than DWLOCs for sulfosate in drinking 
water as a contribution to acute aggregate exposure. Residues of 
sulfosate in drinking water do not contribute significantly to the 
aggregate acute human health risk considering the present uses and uses 
proposed in this action.
    ii. Chronic risk. Using the conservative exposure assumptions 
described above, we conclude that the percent of the RfD that will be 
utilized by aggregate exposure to residues of sulfosate is 30.5% for 
non-nursing infants, the most highly exposed group. The estimated 
average concentrations of sulfosate in surface and ground water are 
less than DWLOCs for sulfosate in drinking water as a contribution to 
chronic aggregate exposure. Residues of sulfosate in drinking water do 
not contribute significantly to the aggregate chronic human health risk 
considering the present uses and uses proposed in this action.

F. International Tolerances

    There are no Codex Maximum Residue Levels established for 
sulfosate.

[FR Doc. 99-8775 Filed 4-7-99; 8:45 am]
BILLING CODE 6560-50-F