Document ID: EPA-HQ-OPP-2007-0116-0002
Agency: epa
Document Type: Supporting & Related Material
Title: 
Posted Date: 2007-04-04T04:00Z

<COMPANY FEDERAL REGISTER DOCUMENT SUBMISSION TEMPLATE  (7/1/2006)>
Dimethenamid-P (BAS 656-PH): new IR-4 crops including winter squash,
pumpkin, radish, turnip, rutabaga, hops. November 28, 2006

<EPA Registration Division contact: [James A. Tompkins at 703-305-5697]>

 

<INSTRUCTIONS:  Please utilize this outline in preparing tolerance
petition documents.  In cases where the outline element does not apply
please insert “NA-Remove” and maintain the outline.  The comment
notes that appear on the left margin represent hidden typesetting codes
designed to expedite the processing of the Federal Register document. 
Please do not remove or alter these comment notes or change the margins,
font, or format in your document. Simply replace the instructions that
appear in italics and brackets, i.e., “[insert company name],” with
the information specific to your action.]>

<TEMPLATE:>

<[Interregional Research Project Number 4 (IR-4)]>

<[PP-06596, 07909, 07697, 07696, 09813, 08705]>

<	21 U.S.C. 346 EPA has received a pesticide petition ([Insert petition
number, PP-xxxxxx]) from [Interregional Research Project Number 4
(IR-4)], [500 College Road East, Suite 201 W, Princeton, NJ, 08540]
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 180.361 by
establishing a tolerance for residues of [the herbicide dimethenamid,
(R,S)-2-chloro-N-[(1-methyl-2-methoxy)
ethyl]-N-(2,4-dimethyl-thien-3-yl)-acetamide)] in or on the raw
agricultural commodity [winter squash, pumpkin, radish roots, radish
tops, turnip roots, turnip tops, turnip greens, rutabaga roots, rutabaga
tops, hops dried cones] at [0.01, 0.01, 0.01, 0.01, 0.01, 0.1, 0.1,
0.01, 0.1, 0.05, respectively,] 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 FDDCA; 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.  [BASF Corporation notes that metabolism in
plants and animals is well understood.]>

<	2. Analytical method. [The proposed analytical method uses extraction
and clean-up followed by quantification with capillary column gas
chromatography using thermionic nitrogen specific detector. A GS/MS
method for identification is also available.  This method is not
selective towards the dimethenamid isomer and is therefore valid for
residues from both racemic dimethenamid and the enriched isomer
dimethenamid-P. Tolerances are proposed based on a non-isomer specific
basis.]>

<	3. Magnitude of residues. [Field trials in major growing areas were
carried out in order to determine the magnitude of residues in the
winter squash, radish, turnip and hop commodities.  EPA has determined
that the petition contains data or information regarding the above
aforementioned crops.  Field trials were conducted in the required
regions.  Field trials were carried out using the maximum number of
applications, the maximum label rate and shortest pre-harvest interval
(PHI).

Dimethenamid-P is the biologically active isomer from the racemic
dimethenamid mixture. The analytical residue method measures both
dimethenamid and dimethenamid-P, so the residue determinations in winter
squash, radish, turnip and hops for dimethenamid-P are considered
representative of the proposed treatments with dimethenamid.

Due to the low levels of residue in the RAC's, tolerances in animal
commodities are not required.]>

<B. Toxicological Profile>

<	1. Acute toxicity.  [Based on available acute toxicity data,
dimethenamid and dimethenamid-P do not pose an acute dietary risk.  The
acute toxicity studies place both technical materials in acute toxicity
category II for acute oral; in acute toxicity category III for acute
dermal, inhalation, and eye; and in acute toxicity category IV for
dermal irritation. The technical materials are both positive skin
sensitizers.]>

<	2. Genotoxicty. [The following testing was performed with dimethenamid
for genotoxicity. A Modified Ames Test: Negative; In Vitro CHO/HGPRT
Mammalian Cell mutation Assay: Negative;  In Vitro Cytogentics - CHO
Cells (1 Study; Chromosome Aberrations): Weakly Positive;  In Vitro UDS
Test Using Rat Hepatocytes (3 Studies; DNA damage and repair): 2
Negative; 1 Equivocally Positive,  Mouse Micronucleus Assay (2 Studies;
Chromosome Aberrations): Negative, Rat Dominant Lethal Assay : 1 study
equivocally positive, 1 study negative.  Overall dimethenamid has been
tested in 14 genetic toxicology assays.  The weight of-the-evidence
demonstrates that dimethenamid is not genotoxic.

The following testing was performed with dimethenamid-P for
genotoxicity. A Modified Ames Test (3 Studies; point mutation):
Negative; In Vitro CHO/HGPRT Mammalian Cell mutation Assay (1 Study;
point mutation): Negative; In Vitro Cytogentics - CHO Cells (1 Study;
Chromosome Aberrations): Negative; In Vitro UDS Test Using Rat
Hepatocytes (1 Study; DNA damage and repair): Negative; Mouse
Micronucleus Assay (1 Study; Chromosome Aberrations): Negative

Dimethenamid-P has been tested in a total of 7 genetic toxicology
assays.  These assays were performed both in vitro and in vivo and
multiple assays were conducted for each of the three EPA Guideline
requirement categories.  Based on the data presented above, the data
indicates that dimethenamid-P does NOT induce gene mutations, is not
clastogenic and does not induce other effects indicative of
genotoxicity.  Therefore, dimethenamid-P does not pose a mutagenic
hazard to humans.]>

<	3. Reproductive and developmental toxicity. [Developmental toxicity -
Rat

A developmental rat study testing dimethenamid via oral gavage at doses
of 0, 50, 215, and 425 mg/kg/day resulted in a development toxicity
NOAEL of 215 mg/kg/day and a maternal toxicity NOAEL of 50 mg/kg/day
based on based on the following: (1) signs of maternal toxicity, in the
form of reduced body weight gain and food consumption, increased liver
weight and clinical observations were observed at dose levels >215
mg/kg/day with an increase in effects to the upper dose level; (2)  at
doses ≥215 mg/kg/day, slight decreases in fetal body weights were
observed and  (3) at the 425 mg/kg/day dose level a slight increase in
resorptions was observed, and two fetuses had incomplete ossified
manubria.  These findings are not indicative of a teratogenic effect and
developmental toxicity was only observed at doses with maternal
toxicity.

A developmental rat study using dimethenamid-P via oral gavage tested at
doses of 0, 25, 150, and 300 mg/kg/day with a development toxicity NOAEL
of 25 mg/kg/day and a maternal toxicity of 25 mg/kg/day based on the
following: (1) signs of maternal toxicity, in the form of decreased body
weights and food consumption were observed at dose levels >150 mg/kg/day
with an increase in effects to the upper dose level; (2) at the 150
mg/kg/day dose level slight decreases in fetal body weights and retarded
ossification of the pelvis pubis were observed; and  (3) at the 300
mg/kg/day dose level slight decreases in fetal body weights,
microphthalmia in two fetuses/two litters, distended ureters, and
retarded ossification of the 2nd sternal centra and pelvis pubis were
observed.  These findings are not indicative of a teratogenic effect and
developmental toxicity was observed only at doses with maternal
toxicity.

Developmental toxicity - Rabbits

A developmental study in rabbits tested dimethenamid via oral gavage at
doses of 0, 37.5, 75, and 150 mg/kg/day (HDT) with a development
toxicity NOAEL of 75 mg/kg/day and a maternal toxicity of 37.5 mg/kg/day
based on: (1) decreased body weight, food consumption, and
absorption/premature delivery in the 75 and 150 mg/kg/day dose groups;
and (2) effects on fetal development including a low incidence of
absorption/premature delivery and an increased incidence of minor
skeletal ossifications in the 150 mg/kg/day dose group.  These findings
are not indicative of a teratogenic effect and developmental toxicity
was observed only at a dose that also demonstrated maternal toxicity.

Reproduction Toxicity:

A two-generation reproduction study using dimethenamid with rats fed
dosages of 0, 7.5, 38, and 155 mg/kg/day (average mg/kg/day dose levels
for both male and female rats) with a reproductive NOAEL of 38 mg/kg/day
and with a parental NOAEL of 38 mg/kg/day based on: (1) parental
toxicity as evident by reduction in body weight and food consumption and
significant increases in absolute and/or relative liver weights in both
males and female rats in the 155 mg/kg/day dose group; and (2)
significant reductions in pup weight during lactation were observed in
the 150 mg/kg/day dose group.  No changes in pregnancy rates, fertility
or length of gestation were observed at all dose levels tested. 

As stated above, the NOAEL of 5 mg/kg/day from the chronic rat study
used to set the RfD is ~8x lower than the maternal NOAEL established in
the rat reproduction study.  Therefore, no additional safety factor is
needed for children.]>

<	4. Subchronic toxicity. [The short-term toxicity of dimethenamid was
investigated in an oral 28-day range-finding study in rats as well as in
3-month studies in rats, mice, and dogs. In addition the short-term
toxicity following dermal exposure was determined in a 21-day study in
rabbits.

The signs of toxicity observed in the three species tested were overall
similar with the liver as the target organ.  The effects observed
typically included the increase in one or more serum liver enzymes and
changes in cholesterol.  Pathology confirmed the liver to be a target
organ. Increased liver weights were observed in all three species
probably indicative of an adaptive response to exposure. 
Histologically, hepatocyte hypertrophy was observed in rats and
hepatocyte vacuolation and dilatation of liver sinusoids occurred in
dogs.

In a 3-week dermal toxicity study in rabbits no substance-related
systemic findings were detected up to the highest dose level tested of
1,000 mg/kg bw.]>

<	5. Chronic toxicity. [Chronic Feeding - Dogs

A 1-year feeding study in dogs fed dimethenamid at dosages of 0, 2, 9.6,
or 49 mg/kg/day with a No-Adverse-Effect Level (NOAEL) of 9.6 mg/kg/day
based on the following effects: (1) slight decreases in body weights for
both the high dose male and female dogs as compared to controls; (2) a
variable degree of periportal hepatocyte vacuolation in the high-dose
male and female dogs; (3) minimal or mild hepatocyte enlargement was
similarly observed in the high-dose dogs; and (4) the liver changes at
the high-dose group correlated with increase in serum alkaline
phosphatase activity and cholesterol levels and increased liver-to-body
weight ratios in both male and female dogs.

Chronic Feeding/Oncogenicity - Rats

A combined chronic feeding/oncogenicity study was performed in rats at
doses of 0, 5.1, 36, and 80 mg/kg/day (males) and 0, 6.8, 49, and 109
mg/kg/day (females) with a NOAEL of 5.1 mg/kg/day (males) and 6.8
mg/kg/day (females) based on the following effects: (1) decreased body
weights in both males and female rat at dose levels >36 mg/kg/day dose
groups with a slight progression of severity to the upper level; (2)
decreased food consumption in both males and female rats at dose levels
>36 mg/kg/day dose groups with a slight progression of severity to the
upper dose level; (3) minimal hematological and clinical chemistry
changes at dose levels >36 mg/kg/day; (4) increased absolute liver
weights for females at dose levels >49 mg/kg/day; (5) microscopic
findings were observed in the liver, parathyroid, and stomach of
high-dose males, only, and  ovaries of high-dose females; and (6) an
increased incidence of benign tumors in the liver of male animals at the
highest dose level tested.  Overall, the slight increase in the benign
liver tumor in high dose males does not indicate that dimethenamid is
carcinogenic.  The increase was not statistically significant, was
within historical control range for Sprague-Dawley rats and was most
likely due to the considerable increase in survival at that dose.

iii.     Oncogenicity - Mice

A carcinogenicity study using dimethenamid in mice tested doses of 0,
3.8, 41, 205, and 431 (HDT) mg/kg/day (males) and 0, 4.1, 41, 200, and
411 (HDT) mg/kg/day (females) with a NOAEL of 41 mg/kg/day for male and
female mice based on the following effects: (1) decreased body weights
and food consumption were observed in both males and female mice at the
highest dose tested; (2) increased liver weights were observed for male
and female mice at the highest dose tested at an interim sacrifice and
increased weights for kidney and liver were observed for female mice at
dose levels >200 mg/kg/day at terminal sacrifice; (3) microscopic
findings were observed in the liver and stomach for both male and female
mice at the upper dose levels; (4) concerning the finding in the
stomach, EPA has determined that this finding was attributed to
irritation of the material and the finding was not toxicology
significant; and (4) no increased incidence of neoplasms occurred at any
dose levels tested in this study.  EPA has concluded that this product
is not oncogenic under the conditions of this study.]>

<	6. Animal metabolism. [Dimethenamid was well absorbed (>90%) and
extensively metabolized by rats.  Excretion was rapid primarily by bile.
 In 7 hr, 45% to 64% of the oral dose was excreted in bile.  By 168
hours after treatment, an average of 90% of the administered dose was
eliminated by all routes.  The radioactivity level in blood decreased
slowly in rat and was associated with some blood components., however,
binding to blood components was demonstrated to not occur in human
blood.  Levels in other tissue after 168 hr were small, and there was no
evidence for a bioaccumulation potential. 

The unchanged dimethenamid in excreta accounted for only 1-2% of the
dose.  There were over 40 metabolites detected in excreta.  Over 20
metabolites were structurally identified by MS and NMR, and confirmed
with the synthesized reference standards.  Metabolism was primarily via
glutathione conjugation pathways.  Dimethenamid was also metabolized via
reductive dechlorination, oxidation, hydroxylation, O-demethylation, and
cyclization.  There was no significant difference in absorption,
distribution, elimination and metabolism between sexes.  There was also
no significant difference in percent absorption between the low dose of
10 mg/kg and the high dose of 1,000 mg/kg, or between the single and
multiple doses.  However, it appeared the elimination via bile was
saturated at 1,000 mg/kg because the elimination via kidney increased
for the high dose.]>

<	7. Metabolite toxicology. [The dimethenamid metabolites M23 and M27
were tested in acute oral toxicity studies and in the Ames mutagenicity
assay and the mouse micronucleus assay.  Both compounds had low acute
oral toxicity with LD50’s greater than 5,000.  Both compounds were
also negative in both the Ames assay and the mouse micronucleus assay.]>

<	8. Endocrine disruption. [No specific tests have been performed with
dimethenamid-P or dimethenamid to determine whether the chemical may
have an effect in humans that is similar to an effect produced by
naturally occurring estrogen or other endocrine effects.  However, there
are no significant findings in other relevant toxicity studies, i.e.
teratology and multi-generation reproductive studies, which would
suggest the dimethenamid produces endocrine related effects.]>

<C. Aggregate Exposure>

<	1. Dietary exposure. [An assessment was conducted to evaluate the
potential risk due to acute dietary exposure of females 13-49 yrs of age
and chronic dietary exposure of the U.S. population and all
sub-populations to residues of Dimethenamid.  Tolerance values that have
previously been established are listed in U.S. 40 CFR § 180.464.   

This analysis included all crops with established tolerance values,
crops pending tolerance assignment (grass grown for seed) and proposed
new crops from IR-4 (including winter squash, pumpkin, radish, turnip,
rutabaga and dried cone hops).  

The dietary assessments were conducted using tolerance level for all
commodities, default processing factors, and 100% crop treated factors. 
These assumptions are conservative because it assumes all commodities
will be at tolerance level and 100% of the crop has been treated with
dimethenamid. Inadvertent residues in animal commodities (i.e. meat,
meat byproducts, milk, eggs) were not considered because studies have
shown that dimethenamid does not accumulate in animal tissues or milk
and tolerance values for these commodities are not required by the
EPA.]>

<	i. Food. [Acute Dietary Exposure Assessment

The EPA has concluded that an acute assessment is only required for
females ages 13-49 years old.  An acute assessment for other
sub-populations is not required.  The acute dietary exposure assessment
was conducted using the Dietary Exposure Evaluation Model software with
Food Commodity Intake Database (DEEM-FCID).  The acute population
adjusted dose (aPAD) used for females 13-49 years of age was 0.75 mg/kg
bw/day.  Using the exposure assumptions discussed above, dimethenamid
acute dietary exposure from food is less than 0.1 % aPAD.  The results
of the acute dietary assessment for females 13-49 years of age are
presented in Table 1.

Table 1.  Results for Dimethenamid Acute Dietary Exposure Analysis Using
DEEM-FCID at the 95th Percentile.  

Population

Subgroups	Exposure Estimate

(mg/kg bw/day)	%aPAD

Females 13-49 years	0.000075	< 0.1

Chronic Dietary Exposure Assessment

A chronic assessment was conducted for all sub-populations.  The chronic
dietary exposure assessment was conducted using the Dietary Exposure
Evaluation Model software with Food Commodity Intake Database
(DEEM-FCID).  The chronic population adjusted dose (cPAD) used for all
sub-populations was 0.05 mg/kg bw/day.  Using the exposure assumptions
discussed above, dimethenamid chronic dietary exposure from food is less
than 0.3 % cPAD for all sub-populations.  The results of the chronic
dietary assessment are presented in Table 2.  

 

Table 2.  Summary of Chronic Dietary Exposure Assessment considering
crops with established and proposed tolerances  for Dimethenamid. 

Population

Subgroups	Exposure Estimate

(mg/kg b.w./day)	%cPAD

U.S. Population	0.00004	0.1

All Infants	0.0000650	0.1

Children 1-2 years	0.0000870	0.2

Children 3-5 years	0.0000870	0.2

Children 6-12 years	0.0000630	0.1

Youth 13-19 years	0.0000440	0.1

Females 13-49 years	0.0000320	0.1

Adults 20-49 years	0.0000330	0.1

Adults 50+ years	0.0000270	0.1

]>

<	ii. Drinking Water. [Since the models used are considered to be
screening tools in the risk assessment process, the Agency does not use
estimated drinking water concentrations (EDWCs) from these models to
quantify drinking water exposure and risk as %PAD.  Instead, drinking
water levels of comparison (DWLOCs) are calculated and used as points of
comparison against the model estimates of a pesticide’s concentration
in water.  A DWLOC is the theoretical upper allowable limit of a
pesticide's concentration in drinking water and is calculated with
considering the aggregate exposure to a pesticide from food and
residential uses. A DWLOC will vary depending on the toxic endpoint,
drinking water consumption, body weights, and pesticide uses. 

Different populations will have different DWLOCs. If the DWLOC is
greater than the model water concentrations, the EPA concludes that
exposure from drinking water is not a risk issue.  The modeled water
concentration is obtained from FIRST model for surface water and SCIGROW
for groundwater.  The values used for comparison to the DWLOC are the
maximum concentrations for any use.  When the EDWC’s are less than the
calculated DWLOCs, EPA concludes with reasonable certainty that
exposures to the pesticide in drinking water would not result in
unacceptable levels of aggregate human health risk. 

Based on the PRZM/EXAMS and SCIGROW models, the EDWCs of dimethenamid
for acute exposure are estimated to be 49 ug/L (ppb) in surface water
and 0.42 ug/L in shallow ground water.  The EDWCs for chronic exposure
are estimated to be 7.9 ug/L in surface water and 0.42 ug/L in shallow
ground water.  The 36-year average of dimethenamid in surface water that
was estimated by PRZM/EXAMS for use in the chronic/cancer risk
assessment is 5.1 ug/L/.  These EDWC values are the maximum modeled
considering all dimethenamid uses.  

Acute Aggregate Exposure and Risk (Food and water)

The aggregate acute risk includes residues of dimethenamid from food and
water.  Exposures from residential uses are not included in the acute
aggregate assessment.  The EDWCs for dimethenamid in surface and ground
water are lower than the DWLOCs for all sub-populations (Table 3).  

Table 3.  Acute Drinking Water Levels of Comparison for Dimethenamid

Population Subgroup	aPAD (mg/kg/day)	Food Exp (mg/kg/day)	Max. Water Exp
(mg/kg/day)	Acute Ground Water EDWC (ug/L)	Acute Surface Water EDWC
(ug/L)	DWLOC (ug/L)

Females 13-49 years	0.75	0.000075	0.749925	49	0.42	22497

The results in the Table 3 demonstrate that there are no safety concerns
for any sub-population based on established and new uses, and that the
results clearly meet the FQPA standard of reasonable certainty of no
harm.  

Chronic Aggregate Exposure and Risk (food and water) 

The aggregate chronic risk includes residues of dimethenamid from food
and water.  Exposures from residential uses are not included in the
chronic aggregate assessment.  The EDWCs for dimethenamid in surface and
ground water are lower than the DWLOCs for all sub-populations (Table
4). 

 

Table 4.  Chronic Drinking Water Levels of Comparison for Dimethenamid

Population Subgroup	cPAD (mg/kg/day)	Food Exp (mg/kg/day)	Max. Water Exp
(mg/kg/day)	Acute Ground Water EDWC (ug/L)	Acute Surface Water EDWC
(ug/L)	DWLOC (ug/L)

U.S. Population	0.05	0.00004	0.04996	7.9	0.42	1749

All Infants (< 1 yr old)	0.05	0.000065	0.049935

	499

Children 1-2 years	0.05	0.000087	0.049913

	499

Children 3-5 years	0.05	0.000087	0.049913

	499

Children 6 – 12 years	0.05	0.000063	0.049937

	499

Youth 13-19 years	0.05	0.000044	0.049956

	1499

Females 13-49 years	0.05	0.000032	0.049968

	1499

The results in Table 4 demonstrates that there are no safety concerns
for any subpopulation based on established and new uses, and that the
results clearly meet the FQPA standard of reasonable certainty of no
harm. 

In summary, we can conclude with reasonable certainty that no harm will
occur from chronic aggregate or acute aggregate exposure to
dimethenamid.

Short- and Intermediate Term Aggregate Exposure and Risk (Food, Water
and Residential Exposure)

Short- and intermediate-term aggregate exposure takes into account
residential exposure plus chronic exposure from food and water. 
Residential exposure is used to refer to non-occupational and
non-dietary exposure.  Dimethenamid is not registered on any sites that
would result in residential exposure.  Therefore, the aggregate risk is
the sum of the risk from food and water, which do not exceed a level of
concern.]>

<	2. Non-dietary exposure. [Dimethenamid is not registered for use on
any sites that would result in residential exposure.]>

<D. Cumulative Effects>

<	[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.’’ 

BASF has considered the potential for cumulative effects of dimethenamid
and other substances that have a common mechanism of toxicity.  BASF is
aware of several other chloroacetanilide herbicides that have been
considered structurally similar to dimethenamid, these being:
acetochlor, propachlor, butachlor, metolachlor, and alachlor.  However,
BASF believes that consideration of a common mechanism of toxicity to
these products is not appropriate or valid.  This conclusion was based
on the presentation EPA made to the EPA FIFRA Science Advisory Panel
(SAP) on March 20, 1997.  The title of the presentation was  
“Grouping of Chloroacetanilide Pesticides Based on a Common Mechanism
of Toxicity.”  In this presentation EPA showed the structure of
several chloroacetanilides that included dimethenamid.  BASF is
identifying Chlor- 7 as dimethenamid.  EPA concluded that Chlor-7 should
not be considered to have a common mechanism to the other
chloroacetanilides based on the following reasons:

Except for Chlor-7 all other members of this case study have a potential
to generate a quinine imine.  The quinone imine intermediate is capable
of reacting with macromolecules.

Chlor-7 has not produced nasal nor thyroid tumors in rats, thus does not
support inclusion in the group for a common mechanism for these tumor
types.

For liver tumors, Chlor-1, Chlor-7, Chlor-5, and Chlor-6, can be
potentially grouped for a common mechanism, but EPA determined that
there is no knowledge of a common mechanism of toxicity or of a common
toxic species responsible for the effect.  Therefore, EPA concluded that
because a mechanism can not be postulated, it believes that sufficient
evidence is not available to support a common mechanism for this tumor
type with these materials.

Therefore, BASF agrees with the position put forward by the Agency and
confirmed by the SAP that a common mechanism is inappropriate for
dimethenamid (Chlor-7) and the other chloroacetanilides mentioned above.
 Therefore, based on the above discussion BASF has considered only the
potential risks of dimethenamid in its exposure assessment.]>

<E. Safety Determination>

<	1. U.S. population. [Based on this risk assessment, BASF concludes
that there is a reasonable certainty that no harm will result to the
general population from the aggregate exposure to dimethenamid
residues.]>

<	2. Infants and children. [Based on this risk assessment, BASF
concludes that there is a reasonable certainty that no harm will result
to infants or children from the aggregate exposure to dimethenamid
residues.]>

<F. International Tolerances>

<	[Maximum residue levels (MRLs) have been established for
Dimethenamid-P and its enantiomer in the registered crops by the Codex
Alimentarius Commission as of January 2006. The recommended MRLs are
0.01 mg/kg and the residue definition could apply to residues arising
from the use of either dimethenamid-P or dimethenamid.]>