[Federal Register Volume 62, Number 228 (Wednesday, November 26, 1997)]
[Notices]
[Pages 63164-63168]
From the Federal Register Online via the Government Publishing Office [www.gpo.gov]
[FR Doc No: 97-30813]


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

ENVIRONMENTAL PROTECTION AGENCY

[PF-777; FRL-5754-4]


Notice of Filing of Pesticide Petitions

AGENCY: Environmental Protection Agency (EPA).

ACTION: Notice.

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

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-777, must 
be received on or before December 26, 1997.

ADDRESSES: By mail submit written comments to: Public Information and 
Records Integrity Branch (7502C), Information Resources and Services 
Division, Office of Pesticides Programs, Environmental Protection 
Agency, 401 M St., SW., Washington, DC 20460. In person bring comments 
to: Rm. 1132, CM #2, 1921 Jefferson Davis Highway, Arlington, VA.
    Comments and data may also be submitted electronically to: <a href="/cdn-cgi/l/email-protection#e7889797caed8388848c8293a78297868a868e8bc9829786c9808891">opp-
<span class="__cf_email__" data-cfemail="bdd9d2ded6d8c9fdd8cddcd0dcd4d193d8cddc93dad2cb">[email protected]</span></a>. 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. 1132 at the 
address given above, from 8:30 a.m. to 4 p.m., Monday through Friday, 
excluding legal holidays.

FOR FURTHER INFORMATION CONTACT: By mail: Joanne Miller (PM 23), 
Registration Division (7505C), Office of Pesticide Programs, 
Environmental Protection Agency, 401 M St., S.W., Washington, DC 20460. 
Office location, telephone number, and e-mail address: Rm. 237, CM #2, 
1921 Jefferson Davis Highway, Arlington, VA 22202, (703 305-6224, e-
mail: <a href="/cdn-cgi/l/email-protection#523f3b3e3e37207c383d333c3c37123722333f333b3e7c3722337c353d24"><span class="__cf_email__" data-cfemail="eb868287878e99c581848a85858eab8e9b8a868a8287c58e9b8ac58c849d">[email protected]</span></a>.

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 supports 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-777] (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:
    <a href="/cdn-cgi/l/email-protection#eb849b9bc68f8488808e9fab8e9b8a868a8287c58e9b8ac58c849d"><span class="__cf_email__" data-cfemail="bdd2cdcd90d9d2ded6d8c9fdd8cddcd0dcd4d193d8cddc93dad2cb">[email protected]</span></a>


    Electronic comments must be submitted as an ASCII file avoiding the 
use of special characters and any form of encryption. Comment and data 
will also be accepted on disks in Wordperfect 5.1/6.1 or ASCII file 
format. All comments and data in electronic form must be identified by 
the docket control number [PF-777] and appropriate petition number. 
Electronic comments on this 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: November 4, 1997.

James Jones,

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

BASF Corporation

PP 6F4604, 4F3041 and FAP 4H5428

    EPA has received pesticide petitions (PP 6F4604, 4F3041, and FAP 
4H5428) from BASF Corporation, 26 Davis Drive, Research Triangle Park, 
P.O. Box 13528, NC 27709, proposing pursuant to section 408 (d) of the 
Federal Food, Drug and Cosmetic Act, 21 U.S.C. 346a(d), to amend 40 CFR 
180.227 by

[[Page 63165]]

establishing and amending tolerances for residues of the herbicide 
dicamba in or on the raw agricultural commodities soybeans, wheat, 
barley, oats, corn, cotton, grasses and asparagus at the proposed 
tolerances as described below. The proposed analytical methods involve 
extraction, partition, clean-up and detection of residues by gas 
chromatography/electron capture detector (gc/ecd). 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. Metabolism is adequately understood on the 
basis of soybean, asparagus, cotton, sugarcane and published data on 
grass. In the majority of registered crops, the major metabolite is the 
3,6 dichloro-5-OH-o-anisic acid. Tolerances are expressed as the 
dicamba parent plus the respective major metabolite.
    2. Analytical method. BASF Corp. has provided suitable 
independently validated analytical methods for detecting and measuring 
levels of dicamba and its metabolites in or on food with a limit of 
detection that allows monitoring of food with residues at or above the 
levels described in these and the existing tolerances. Adequate methods 
are available in PAM-II for enforcement purposes. The analytical method 
involves extraction, partition, clean-up and detection of residues by 
gas chromatography/electron capture detector (gc/ecd).
    3. Magnitude of the residue--i. Plant. Residue trials have been 
conducted with dicamba on the crops for expanded use requested in the 
subject petitions. Multiple salts of dicamba were studied in side-by-
side testing to confirm that no effect on magnitude of the residues was 
caused by the salt formulation type of the dicamba. The tolerances 
listed below are based on the maximum expected residue from 
geographically representative field trial data:
    Proposed tolerances for combined residues of the herbicide dicamba 
(3,6-dichloro-o-anisic acid) and its metabolite 3,6-dichloro-5-hydroxy-
o-anisic acid in or on the raw agricultural commodities as follows 40 
CFR 180.227(a): Cottonseed 3.0 parts per million (ppm); Corn, forage 
3.0 ppm; Corn, fodder 3.0 ppm; Crop Group 17, Grass forage, fodder and 
hay Forage 125 ppm, Hay 200 ppm; Wheat, forage 80 ppm, Wheat, hay 20 
ppm; 21 U.S.C. section 701 MRL Cottonseed meal 5.0 ppm; Wheat grain 2 
ppm, Wheat straw 30 ppm; Barley grain 2 ppm; Barley straw 30 ppm.
    Proposed tolerances for combined residues of the herbicide dicamba 
(3,6-dichloro-o-anisic acid) and its metabolite 3,6-dichloro-2-
hydroxybenzoic acid in or on the raw agricultural commodities as 
follows 40 CFR 180.227(b): Soybean grain 4 ppm, Soybean hulls 13 ppm; 
Asparagus 3.5 ppm.
    Only newly generated data, or data not implicated in the CRAVEN 
Laboratories indictment are used to support the subject petitions.
    Dicamba residues concentrate in the following commodities: soybean 
hulls; sugarcane molasses; cottonseed meal.
    ii. Animal. The amended uses proposed do not yield secondary 
residues in meat and milk above the tolerances already published under 
40 CFR 180.227. Data from metabolism and feeding studies in poultry 
have established that the maximum expected dietary burden from crops 
treated with dicamba will not result in quantifiable residues above the 
limits of the analytical method.

B. Toxicological Profile

    Data are provided that are representative of the mammalian toxicity 
effects of dicamba and are part of the many studies conducted to 
support the BASF Corp. assertion of safety of dicamba to humans.
    1. Acute toxicity--i. Oral Rat LD<INF>50</INF>: 1,879 mg/kg (m); 
1581 mg/kg (f).
    ii. Acute Dermal Rat LD<INF>50</INF>: > 2,000 kg/kg (m/f).
    iii. Acute Inhalation Rat LC<INF>50</INF>: > 9.6 mg/L (m/f).
    iv. Primary Eye Irritation: Extremely irritating and corrosive to 
the eye.
    v. Primary Dermal Irritation Rabbits: Not a primary skin irritant.
    vi. Dermal Sensitization Guinea Pigs: Moderate potential to cause 
dermal sensitization.
    vii. Acute Neurotoxicity: NOEL <300 mg/kg (lowest dose tested). 
Neurobehavioral effects were observed at all dose levels but primarily 
at the initial 1.5 hr post-dose testing only. No neurobehavioral 
effects were noted by day 14 after treatment and no neuropathological 
effects were found indicating there are no persistent effects on the 
nervous system.
    2. Genotoxicity. Ames: Negative; In vitro chromosome aberration in 
Chinese Hamster Ovary: Negative; Sex-linked recessive lethal in 
Drosophila: Negative; Chromosome aberrations in rat bone marrow: 
Negative; Mitotic recombination: Negative; UDH (UDS with WI-38 human 
lung fibroblasts: Negative; DNA damage as detected with repair 
deficient prokaryote E. coli: Positive; DNA damage as determined with 
repair deficient eukaryote S. typhimurium: Negative; UDS in human lung 
lymphocytes with activation: Negative; Sister chromatid exchange in 
human cultured lymphocytes: slight increase. Overall weight of the 
evidence from all studies indicates that dicamba is not genotoxic.
    3. Reproductive and developmental toxicity--i. Rodent developmental 
toxicity rat. Oral doses of 0, 64, 160, or 400 mg/kg were administered 
daily during gestation days 6 to 19. Maternal toxicity occurred at the 
high dose as evidenced by mortality of four animals, clinical signs and 
decreased weight gain. The numbers of implantations, resorptions, and 
fetuses for test animals were similar to those numbers for control 
animals. No fetal abnormalities were attributed to exposure to dicamba. 
Therefore, technical dicamba was not found to be teratogenic. Maternal 
toxicity was found only at the HDT with a NOEL of 160 mg/kg/day. The 
developmental NOEL was the highest dose tested of 400 mg/kg/day.
    ii.  Rabbit developmental toxicity. Dicamba was administered orally 
(undiluted) via capsule to groups of 20 artificially inseminated New 
Zealand White rabbits at dose levels of 0, 30, 150, or, 300 mg/kg on 
days 6-18 of presumed-gestation. Females were sacrificed on Day 29 of 
presumed gestation. Maternal toxicity occurred at 150 and 300 mg/kg/day 
as evidenced by clinical signs and either body weight loss or reduced 
weight gain. Abortions occurred at 150 and 300 mg/kg/day. No 
significant differences were obtained in litter averages for corpora 
lutea, implants, litter sizes, resorption sites, percent male fetuses, 
fetal body weight, percent resorbed conceptuses or number of does with 
any resorptions. No gross external, soft tissue or skeletal alterations 
in fetuses were considered to be related to treatment. Therefore, 
dicamba was found to be not teratogenic. The maternal no-observed-
adverse-effect-level (NOAEL) for technical dicamba to pregnant rabbits 
was 30 mg/kg/day. Levels of 150 and 300 mg/kg caused abortions, but 
were at significant maternally toxic doses. The developmental NOAEL was 
the highest dose tested, 300 mg/kg/day.
    iii. Two-generation reproduction rat. Potential effects on growth 
and reproductive performance were assessed over 2-generations of rats 
maintained on diets containing Technical Dicamba at concentrations of 0 
(control), 500, 1,500,

[[Page 63166]]

or 5,000 ppm. Parental toxicity occurred at 5,000 ppm in the form of 
lower weight gain in females and increased liver weights of both sexes. 
Exposure at 5,000 ppm was associated with a slower growth rate of F1 
pups prior to weaning and resulted in lower initial body weights in 
those selected as parental animals. The lower body weight was 
associated with a decrease in both food consumption and water intake. 
Sexual maturation was slightly delayed among males, but was likely 
associated with the initial reduced growth rate. F2 pup weights were 
reduced at 3,000 and 1,500 ppm. There were no treatment-related effects 
on reproductive ability at any level. The NOEL and LOEL for systemic 
toxicity were 1,500 (approx. 130 mg/kg/day) and 5,000 ppm, 
respectively. The NOEL and LOEL for pup toxicity were 500 (approx. 45 
mg/kg/day) and 1,500 ppm, respectively.
    4. Subchronic toxicity--i. Twenty-one-day Dermal. Technical dicamba 
was applied dermally to rabbits for 5 days a week for three weeks at 
dosage levels of 0, 100, 500 and 2,500 mg/kg/day. There were no 
systemic effects at any level of treatment. Skin irritation was evident 
at all treatment levels, but consisted of only a slight erythema at 100 
mg/kg/day. The systemic NOEL was the highest dose tested of 2,500 mg/
kg/day.
    ii. Thirteen-week rodent feeding (rat). Rats were offered technical 
dicamba at dietary concentrations of 0, 1,000, 5,000, or 10,000 ppm. 
The mean body weight and food consumption values for the high dietary 
level animals were decreased from the control values. No adverse 
treatment-related findings were noted in either the blood parameters 
investigated or necropsy evaluation. Microscopic examinations of the 
liver revealed an absence or reduction of cytoplasmic vacuolation in 
the hepatocytes of the high dietary level animals. The NOEL was 5,000 
ppm (342 mg/kg/day males, 392 mg/kg/day females).
    iii. Thirty-eight-week non-rodent (dog). In a dose-range finding 
study for a subsequent chronic dog study, a small number of dogs were 
treated via the feed with technical dicamba at dosage levels of 0, 
1,000, 2,500 and 5,000 ppm for four to eight weeks. Decreased food 
consumption occurred in all dose groups during the first week of 
treatment, and persisted in some dogs at 2,500 and 5,000 ppm. Decreased 
body weight gains or weight loss were noted in the treatment groups. 
The NOEL from the one-year dog study discussed below is used to satisfy 
the requirement for the subchronic dog NOEL.
    iv. Sub-chronic neurotoxicity. Rats were fed technical dicamba for 
13 weeks at dosage levels of 0, 3,000, 6,000 and 12,000 ppm. Body 
weights were slightly reduced in high dose animals. Neurobehavioral 
effects were noted at the high dose and consisted primarily of signs 
associated with rigidity in response to handing. No histopathological 
effects on the peripheral or central nervous system were noted. The 
neurotoxicity NOEL was established at 6,000 ppm (401 mg/kg/day males, 
and 472 mg/kg/day, females).
    5. Chronic toxicity--i.  Chronic toxicity-dog. Technical Dicamba 
was offered orally at dietary concentrations of 0 (Control), 100, 500, 
or 2,500 ppm to dogs for 1 year. Initially, a decrease in food 
consumption was noted mainly among males at 500 and 2,500 ppm. This was 
most notable in a single 2,500 ppm male resulting in almost no food 
consumed for the 1st 3 weeks of feeding. Following administration of 
the 2,500 ppm diet in a water slurry during weeks 4-6, this male was 
placed back on feed and food consumption stabilized. There appears to 
be a limit to the amount of material that can be added to the feed 
before dogs will not consume the diet. The 2,500 ppm level was 
considered close to the maximum that could be employed, as 1 dog failed 
to consume the diet when offered in the usual form. Due mainly to the 
aforementioned male, mean body weight of 2,500 ppm males did not 
increase until week 5. The overall body weight gain for the 1 year 
period was comparable for all groups. It was concluded that aside from 
the lower food consumption, there were no effects due to treatment with 
dicamba. The no-effect level for toxicity was the highest dose tested 
of 2,500 ppm (approx. 59 mg/kg/day males, 57 mg/kg/day females).
    ii. Chronic feeding/oncogenicity in rat. Groups of 60 rats/sex were 
maintained on diets containing technical dicamba at concentrations of 
either 0, 50, 250, or 2,500 ppm. An interim sacrifice of 10/sex/level 
was conducted at 12 months. Initially scheduled as a 27 month (108 
week) study, males were sacrificed at 115 weeks and females at 118 
weeks due to high survival rates.
    There were no effects due to treatment on any chronic toxicity 
parameters investigated. In males, no statistically significant 
differences in data for all tumors combined, all benign tumors 
combined, and all malignant tumors combined were obtained. A slight 
increase in malignant lymphoma was not statistically significant 
(pairwise comparisons) and was not considered to be toxicologically 
significant. A slight increase in thyroid parafollicular cell carcinoma 
in the high treatment group was noted but was not statistically 
significant in pairwise comparisons. In females, no statistically 
significant differences were noted in comparisons with all tumors 
combined, all benign tumors combined, and all malignant tumors combined 
or in any individual tumor type.
    In summary, no signs of toxicity related to administration of 
dicamba were noted. Dicamba was not oncogenic. Based on the results of 
the study, the no effect level was considered to be 2,500 ppm (107 mg/
kg/day males and 127 mg/kg/day females).
    iii. Oncogenicity in mice. Groups of mice were fed diets containing 
dicamba at concentrations of 0, 50, 150, 1,000, or 3,000 ppm. Males 
were killed following 89 weeks of feeding and females were killed 
following 104 weeks of feeding. Reduced body weight gain (not 
statistically different) was noted among 3,000 ppm females. Increased 
mortality noted among 3,000 ppm males was considered unlikely to be 
related to treatment but could not be completely excluded. An increased 
incidence in lymphoid tumors, showing a statistical significance at 150 
and 1,000 ppm, occurred in females. However, the incidence at 3,000 ppm 
did not statistically differ from control. Additionally, there was no 
significant trend with dosage and the values for treated females were 
within historical control data. The incidence of benign and malignant 
tumors in all tissues were similar for treated and control animals. The 
NOEL was determined to be 1,000 ppm (108 mg/kg/day in males and 121 mg/
kg/day in females). However, the RfD best committee chose to establish 
the NOEL at 3,000 ppm and stated that no LOEL had been established.
    6. Estrogenic or other endocrine effects. No specific tests have 
been conducted to determine endocrine-disrupting effects. However, 
extensive subchronic and chronic tests have been conducted in several 
species, and results have demonstrated no effects on the endocrine 
system.
    7. Animal metabolism. Dicamba has been tested in rats, dogs, 
cattle, goats and hens. In all cases, dicamba is excreted very rapidly, 
mainly as unchanged dicamba and to a lesser extent as 3,6-dichloro-2-
hydroxybenzoic acid with trace amounts of 3,6-dichloro-5-hydroxy-o-
anisic acid. The results of these studies demonstrate that dicamba is 
not persistent and does not accumulate in animals.
    8. Metabolite toxicity. Toxicity of the metabolites of dicamba to 
humans is concurrently evaluated during toxicity testing because both 
plant and animal

[[Page 63167]]

metabolites are formed during the course of toxicity tests. Both plant 
and animal major metabolites are considered not of toxicological 
concern.

C. Aggregate Exposure

    1. Dietary exposure. Exposure from the use of Dicamba in the 
culture of wheat, barley, oats, millet, sorghum, corn, soybeans, 
grasses, cotton, sugarcane and asparagus crops is discussed under the 
below topics of food and drinking water.
    2. Food. The subject petition amends these uses but does not add 
new crops. The potential dietary exposure of the population to residues 
of dicamba or its metabolites is calculated based on the Theoretical 
Maximum Residue Contribution (TMRC) for all crops with dicamba use. The 
TMRC is a worst case estimate of dietary exposure since it assumes that 
100 percent of all crops for which tolerances are established are 
treated with dicamba, and that pesticide residues are present at the 
tolerance levels. The resulting dietary exposure estimate therefore 
overestimates exposure and is considered conservative. The number is 
then determined to be a percentage of the EPA decided Reference Dose 
(RfD). Dietary exposure may occur from crop commodities and meat and 
milk. Based on the EPA DRES model BASF Corp. has estimated that the 
average US population dietary exposure to dicamba to be only 1.87% 
percent of the RfD. This number is very low and considered very safe as 
an active ingredient is allowed up to 100% before less conservative 
risk assessment measures are initiated.
    Acute dietary analysis compared the daily dietary exposure to the 
lowest NOEL for acute and subchronic studies. EPA's current policy for 
Tier I analysis uses the conservative assumption that all residues are 
at a high end estimate or maximum, typically taken as the tolerance 
value. Acute dietary assessment for dicamba is made by comparing the 
ratio of exposure and the NOEL from acute neurotoxicity of 300 mg/kg/
day to achieve a Margin of Exposure (MOE). A MOE of 300 is required 
because a NOEL was not reached in the acute neurotoxicity test. The 
following MOE values are obtained for key population subgroups.


                                                                        
------------------------------------------------------------------------
            Population Subgroup                   Margin of Exposure    
------------------------------------------------------------------------
US Population                                6000                       
Infants <1 year                              3000                       
Children 1 to 6                              3000                       
Females 13+ years                           17000                       
Males 13+ years                              10000                      
------------------------------------------------------------------------


    3. Drinking water. Dicamba has been used commercially for in excess 
of 30 years. From available public data, detections in ground water 
from commercial uses have been very low and infrequent. The typical 
level found in ground water is less than 5 ppb. This should be compared 
to the current Health Advisory Level (HAL) of 200 ppb and the 
anticipated HAL of 3,000 ppb under the newly revised RfD of 0.45 mg/kg/
d.
    These infrequent and low levels of detection in groundwater 
demonstrate that significant movement of dicamba is not likely and is 
not a considerable factor in assessing human health risk.
    4. Non-dietary exposure. Non-dietary exposure would mainly occur 
from the use of dicamba for broadleaf weed control on residential or 
recreational turf. BASF is currently collecting data on the potential 
exposure from non-dietary sources such as residential turf use. 
However, no reliable information is currently available for risk 
assessment at this time. This petition is only related to already 
approved crop uses and therefore non-dietary route of exposure is not 
considered to be a factor in assessing additional human risk.

D. Cumulative Effects

    Dicamba belongs to the benzoic acid class of compounds. There are 
no other compounds of this class in significant use and none in food 
use. Therefore, cumulative effects from dietary or non-occupational 
exposure from pesticides of similar chemistry are considered unlikely. 
BASF Corp. does not have reliable data to indicate a common mechanism 
of toxicity to other compounds. Therefore cumulative effects from 
common mechanisms of action are also unlikely.

E. Safety Determination

    The RfD for dicamba is 0.45 mg/kg/d. The RfD is a level at or below 
which daily aggregate exposure over a lifetime will not cause 
appreciable human health risk. The estimates of exposure are based on 
conservative assumptions that all crops with a tolerance for dicamba 
are treated and that all residues found are at the maximum or tolerance 
level.
    1. U.S. population. Using the conservative assumptions described 
above, BASF Corp. has estimated that the US population dietary exposure 
to dicamba is 1.87% percent of the RfD.
    2. Infants and children. Dicamba was not teratogenic in either rats 
or rabbits despite testing to maternally toxic doses. No developmental 
toxicity was observed in rats and the only effect observed in rabbits 
were abortions at clearly maternally toxic doses. Dicamba produced no 
effects on reproduction in a 2-generation study in rats. The only 
effect observed was a decrease in pup body weight at the high dose 
which also produced parental toxicity, and at the mid-dose that was 
relatively high (130 mg/kg/day). Based on the weight of evidence from 
all reproductive and developmental studies, no selective toxic efects 
on infants and children are expected, and no additional safety factor 
is warranted.
    Using the conservative assumptions described above, BASF Corp. has 
estimated the dietary exposure to infants and children as percent of 
the RfD. From the current and new proposed use of dicamba dietary 
exposure for the most sensitive subgroups are 6.65% for non-nursing 
infants (<1 yr old) and 4.6% for children 1 to 6 yrs old.
    Aggregate exposure due to the combined residues in food, drinking 
water and non-dietary exposure through direct contact with residues in 
a residential setting (lawn) should be pursued through the use of a 
reserve risk approach. The elements for consideration are therefore 
estimated as follows:

Food:  Total Population . . . . . .1.87%
Non-nursing Infants <6 yrs . . . 6.7%
Water/Lawn:  Low human risk. . . . . .
expected to be inconsequential

    BASF Corp. believes that the water and non-dietary exposure risk 
for the most sensitive subgroup is inconsequential due to demonstrated 
low findings in water relative to the HAL and low toxicity to humans 
with respect to oral, dermal and inhalation exposure.
    Aggregate exposure is therefore estimated to be less than 10% of 
the RfD for the most sensitive population subgroup. Therefore, BASF 
Corp. concludes that there is reasonable certainty that no harm will 
result from aggregate exposure of residues of dicamba or its 
metabolites including all dietary and other non-occupational exposures.

[[Page 63168]]

F. International Tolerances

    No international tolerances have been established under CODEX. 
Therefore there is no need to ensure consistency.
[FR Doc. 97-30813 Filed 11-25-97; 8:45 am]
BILLING CODE 6560-50-F


</pre><script data-cfasync="false" src="/cdn-cgi/scripts/5c5dd728/cloudflare-static/email-decode.min.js"></script></body>
</html>