	

EPA Registration Division contact: Barbara Madden, (703) 305-6463	

Interregional Research Project No. 4

PP# 0E6209

227 by establishing a tolerance for combined residues of the herbicide
dicamba (3,6-dichloro- o -anisic acid) and its metabolite
3,6-dichloro-5-hydroxy- o- anisic in or on the raw agricultural
commodities Corn, sweet, kernel plus cob with husks removed at 0.04 
ppm; Corn, sweet, forage at 0.50 ppm; and Corn, sweet, stover at 0.50
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.

	.

                                      

. The 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. 

. 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).

. Residue trials have been conducted with dicamba/diflufenzopyr end use
product Distinct on the sweet corn crop for expanded use requested in
the subject petition.  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): Corn, sweet, kernel plus cob
with husks removed at 0.04 ppm; Corn, sweet, forage at 0.05 ppm; and
Corn, sweet, stover at 0.05 ppm.  

 

             	 4.  Animal residue.  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.

.  Dicamba has been evaluated for genotoxicity in numerous in vitro and
in vivo studies.  The results are:  Ames assay (3 studies point
mutation): negative; mammalian cell mutagenicity with L5178Y mouse
lymphoma cells (3 studies; point mutation): negative; in vitro
chromosome aberration test in Chinese Hamster Ovary (CHO) cells (1 test
chromosome aberration): negative; in vivo mouse micronucleus assay (2
studies chromosome aberration): negative.  It is concluded that dicamba
is not genotoxic. 

. Administration of dicamba to pregnant rats at dose levels of 0, 64,
160, and 400 mg/kg resulted in maternal toxicity at the highest dose
level as indicated by mortality, clinical signs (e.g. ataxia, decreased
motor activity, stiff body when held), and decreased body weight gain
and food consumption. Based on these findings, the maternal no observed
effect level (NOAEL) was 160 mg/kg in this study. In the absence of any
developmental toxicity, the developmental NOAEL was 400 mg/kg bw/day.

Administration of dicamba at dose levels of 0, 30, 150 and 300 mg/kg to
pregnant rabbits during days 6 to 18 of gestation resulted in maternal
toxicity at dose levels ( 150 mg/kg as indicated by mortality, body
weight loss, reduced food consumption, and an increased incidence of
abortions at 300 mg/kg and clinical observations (ataxia and decreased
motor activity) at ( 150 mg/kg. Irregular ossification of nasal bones of
the skull in fetuses was observed at 300 mg/kg bw/day.  The maternal
NOAEL was determined to be 30 mg/kg bw/day and the developmental NAOEL
was determined to be 150 mg/kg bw/day.

In a two-generation study rat reproduction toxicity study, dietary
administration of dicamba at dose levels of 0, 500, 1500, and 5000 ppm
resulted in slight parental toxicity at 5000 ppm as indicated by
decreased body weight gain of F0 and F1 females during gestation,
clinical signs of F1 females during lactation (increased body tone and
slowed righting reflex), as well as by increased liver weights in F0 and
F1 adults. The increased liver weights were, however, not accompanied by
any histopathological findings. Reproductive performance was not
affected by treatment.  Developmental toxicity was observed as reduced
pup weights in the top dose group of 5000 ppm at birth and reduced body
weight gain at 1500 and 5000 ppm. Secondary to the initially lower F1
pup weights, a slight delay of sexual maturation was observed in F1
males. The parental toxicity NOAEL was 1500 ppm (approximately 122 and
136 mg/kg bw/day for males and females, respectively).  Based on the
effects on pup body weight gain at 1500 ppm the NOAEL for developmental
toxicity was 500 ppm (equivalent to a daily dose of approx. 45 mg/kg
bw/day). There were effects on reproduction up to the highest dose
tested (5000 ppm, approx. 350 mg/kg bw/day).

  

Subchronic toxicity.  Administration of dicamba to rats at dietary
concentrations of 0, 500, 3000, 6000, and 12000 ppm for three months
resulted in a marked decrease of body weight gain and reduced food
consumption at the highest dose level. The liver was identified as
target organ as indicated by an increased activity of hepatic enzymes,
altered liver associated clinical chemistry parameters, increased
relative liver weights as well as hepatocyte hypertrophy and
pigmentation.. In addition, a number of minor hematological changes were
seen at the high dose. Except for the increased serum phosphate levels
all observed changes were shown to be reversible within 28 days upon
cessation of compound administration. Based on the results of the study,
the NOAEL for subchronic toxicity was determined to be 6000 ppm
(approximately 500 mg/kg bw/day).  

Dogs were treated with dicamba at dose levels of 0, 10, 50 and 300
mg/kg/day for 13-weeks. Treatment at a dosage of 300 mg/kg/day resulted
in effects on gait and behavior, decreased food intake and body weight
gain, minor alterations in the red blood cell parameters and
disturbances in the serum lipid levels. Treatment at a dosage of 50
mg/kg/day resulted in slightly decreased serum lipid levels, which were
considered not to be adverse. Therefore, the NOAEL was 50 mg/kg bw/day.

A dermal toxicity study administered dicamba at doses up to 1000 mg/kg
bw/day for 21 days to male and female rabbits.  There was no evidence of
systemic toxicity at any dose.  Therefore, the NOAEL for systemic
toxicity in this study is considered to be 1000 mg/kg/day.

. Dietary administration of dicamba to rats at concentrations of 0, 50,
250 and 2500 ppm for up to 27 months resulted in no adverse effects up
to the highest dose level.  Based on the results of the study, the NOAEL
was 2500 ppm (approximately 107 mg/kg bw/day). There was no evidence of
oncogenic potential in this study.

The top dose of 2500 ppm equivalent to 107 mg/kg bw/day selected for the
chronic rat study can be justified by a pharmacokinetic study. In this
study a saturation of elimination processes was reached at dose levels
of 100 mg/kg bw for females and between 100 and 200 mg/kg bw for males. 
Testing above the level of 107 mg/kg bw/day in the rat cancer study
would not be appropriate. Continued treatment at doses in excess of
where saturation of excretion occurs would result in a physiological
condition that is irrelevant for human exposure at doses below the
saturation point and most likely result in excessive kidney and liver
toxicity.

Dicamba was administered to mice via the diet at dose levels of 0, 50,
150, 1000, and 3000 ppm for at 24 months.   A statistically significant
increase in male mortality and a slight body weight gain reduction was
observed in high dose animals. All other parameters of systemic toxicity
were unaffected. Based on these data, the NAOEL in this study was 1000
ppm (approximately 115 mg/kg/day). There was no evidence of oncogenic
potential.

Dietary administration of dicamba to dogs for one year at dietary dose
levels of 0, 100, 500, and 2500 ppm did not result in any systemic
toxicity. The dose of 2500 ppm is near to the limit content of dicamba
in the diet which dogs will consume. Based on the result of this study,
the NOAEL was 2500 ppm (approx. 52 mg/kg bw/day).

.  In oral pharmacokinetic and metabolism studies in rats, dicamba was
rapidly absorbed and then efficiently and rapidly eliminated mainly via
urinary excretion.  Maximum blood concentrations were reached within one
hour and then declined very rapidly with a half-life time of 1.1 to 2.1
hours.  The absorbed radioactivity was rapidly and almost completely
excreted via urine (85-98% of applied dose within 24 hours). A recent
pharmacokinetic study in rats revealed that the renal excretion is
saturated at higher dose levels (( 100 - 200 mg/kg bw). A low percentage
of the dose administered was eliminated in the feces (1 to 2 % of
applied). Total radiocarbon in the body was generally very low. Tissue
levels were low (max. 4.5 ppm after 16 hours) and declined rapidly (max.
0.14 ppm after 96 hours). Kidneys contained the highest residue levels
(which is in accordance with the urinary excretion of dicamba) followed
by blood and liver. No accumulation of dicamba was observed.  The parent
dicamba was metabolized only to a limited degree and represented the
major radiocarbon fraction in urine, feces and examined tissues. In the
urine, 3,6-dichloro-2-hydroxybenzoic acid was found in small quantities.
The glucuronide of dicamba and the metabolite, 5-hydroxy dicamba (5-OH
dicamba) were also found at low levels in rat urine.

	

Metabolite toxicology. All significant plant metabolites were also found
in the rat metabolism studies. However, 5-OH dicamba,  which represents
a significant metabolite in several plants, was detected in rats at low
amounts only. Therefore, additional studies were conducted to
investigate the toxicological profile with this metabolite. The
metabolite 5-OH dicamba was not acutely toxic. A series of genotoxicity
studies were conducted including an Ames mutagenicity test, mouse
lymphoma mammalian cell mutagenicity test, in vitro chromosome
aberration in CHO cells, mouse micronucleus in vivo chromosome
aberration and an in vivo Unscheduled DNA synthesis (UDS) test in rats. 
Most studies were negative.  In an in vitro mammalian cell mutagenicity
assay, a positive response was obtained without metabolic activation. 
The increased incidence of mutations occurred only at doses which were
cytotoxic.  A positive was also observed in an in vitro chromosome
aberration study.  However, an in vivo micronucleus assay was negative. 
The weight of the evidence is that the 5-OH metabolite of dicamba is not
genotoxic.

.  No specific tests have been conducted with dicamba to determine
whether the chemical has a potential for endocrine disruption.  However,
there were no significant findings in other relevant toxicity studies
(i.e., subchronic and chronic toxicity, teratology and multi-generation
reproductive studies) which would suggest that dicamba produces
endocrine related effects.

However, signs of neurotoxicity (e.g. ataxia, rigid when handled,
impaired righting reflex) were observed in the developmental toxicity
studies. Therefore acute and subchronic neurotoxicity studies in rats
were conducted 

The single oral administration of dicamba at dose levels of 0, 300, 600,
and 1200 mg/kg bw to rats resulted in one case of mortality and
decreased mean body weight gain and food consumption in high dose males.
Dose dependent neurobehavioral effects were apparent in all treated
groups at 1.5 ± 1 hours after dosing. The overall effect of treatment
is best described as a stimulus- or stress-induced rigidity. At the day
14 neurobehavioral examination the dicamba-treated animals were
performing similarly to vehicle control animals, indicating that the
neurobehavioral changes were transient. The transient nature of the
neurotoxic effects is also substantiated by the absence of any
treatment-related neurohistopathological findings.  The NOAEL was
determined to be <300 mg/kg bw/day.

Dietary administration of technical dicamba to rats at dietary dose
levels of 0, 3000, 6000, and 12000 ppm for 3 months resulted in a
slightly decreased body weight gain in high dose animals. The main
effect on body weight gain was observed in treatment week one with males
more affected than females. Cumulative food consumption was slightly
decreased in high dose males. The major neurobehavioral
treatment-related effect in the high-dose animals was an increased
frequency of rigid body tone when handled at weeks 4, 8, and 13. Despite
the persistence of these neurobehavioral findings throughout the study,
administration of dicamba did not cause damage to the nervous tissues as
indicated by the histopathology findings.  The NOAEL was determined to
be 401 and 472 mg/kg bw/day (males and females, respectively).

. Exposure assessments were conducted to evaluate the potential risk due
to acute and chronic dietary exposure of the U.S. population to residues
of dicamba.  This herbicide and its metabolite
(3,6-dichloro-5-hydroxy-o-anisic acid; DCSA), in or on raw agricultural
commodities, and metabolites in or on animal fat, liver, meat and meat
byproducts were expressed as the parent compound.  The tolerance values
previously established for various cereals, asparagus, sugarcane,
cotton, and animal products are listed in the U.S. 40 CFR § 180.227. 
This analysis included all current tolerances and the proposed tolerance
values for sweet corn (0.04 ppm kernel plus cob with husk removed; 0.05
ppm for stover and forage).

Acute Dietary Exposure Assessment

The acute dietary exposure estimates were based on tolerance values,
default process factors, 100% crop treated values for all commodities
including the currently registered and proposed uses.  The consumption
data was from the USDA Continuing Survey of Food Intake by Individuals
(CSFII 1994 - 1996, 1998) and the EPA Food Commodity Ingredient Database
(FCID) using Exponent's Dietary Exposure Evaluation Module (DEEM-FCID)
software.  

The acute population adjusted dose (aPAD) used for all sub-populations
was 1.0 mg/kg bw/day.   Considering the exposure assumptions discussed
above, dicamba acute dietary exposure from food is less than 6 % aPAD
for the U.S. population and all sub-populations.  The results of the
acute dietary assessment are presented in Table 1.

Table 1.	Results for Dicamba Acute Dietary Exposure Analysis Considering
all Current Tolerances and the Proposed Tolerances for Sweet Corn using
DEEM-FCID at the 95th Percentile 

Population	Exposure Estimate	%aPAD

Subgroups	(mg/kg b.w./day)*	 

U.S. Population	0.029757	3.0

All Infants (< 1 year old)	0.051651	5.2

Children (1-2 years old)	0.053779	5.4

Children (3-5 years old)	0.048466	4.8

Children (6-12 years old)	0.035541	3.6

Youth (13-19 years old)	0.023578	2.4

Females (13-49 years old)	0.021483	2.1

Adults (20-49 years old)	0.015067	1.5

Adults (50+ years old)	0.018052	1.8

aPAD = acute population adjusted dose 

* Exposure Estimate (95th percentile) was based on tolerance values,
default processing factors, and considering 100% crop treated for all
commodities 

Results of the analysis show that for the U.S. population and all
sub-populations, the exposures are below the Agency's level of concern
(< 100% aPAD).  Additional refinements in the dietary risk assessment
(i.e. utilizing anticipated residue values, process factors, percent
crop treated values) would further reduce the estimated exposure values.
 

Chronic Dietary Exposure Assessment

The chronic dietary exposure estimates were based on tolerance values,
default process factors, and 100% crop treated values for all currently
registered and proposed uses.  The consumption data was from the USDA
Continuing Survey of Food Intake by Individuals (CSFII 1994 - 1996,
1998) and the EPA Food Commodity Ingredient Database (FCID) using
Exponent's Dietary Exposure Evaluation Module (DEEM-FCID) software.  The
tolerance values included the proposed values for sweet corn.  

The chronic population adjusted dose (cPAD) used for U.S. population and
all sub-populations is 0.45 mg/kg bw/day. Considering the exposure
assumptions discussed above, dicamba chronic dietary exposure from food
for the U.S. population was < 7% of the cPAD.  The most highly exposed
population sub group was children 1-2 years of age at 6.5% cPAD.   The
results of the chronic dietary assessment are presented in Table 2. 

Table 2. 	Results for Dicamba Chronic Dietary Exposure Analysis
Considering all Current Tolerances and the Proposed Tolerances for Sweet
Corn using DEEM-FCID

Population	Exposure Estimate	%cPAD

Subgroups	(mg/kg b.w./day)	 

U.S. Population	0.011574	2.6

All Infants (< 1 year old)	0.018928	4.2

Children (1-2 years old)	0.029346	6.5

Children (3-5 years old)	0.026702	5.9

Children (6-12 years old)	0.018314	4.1

Youth (13-19 years old)	0.0112	2.5

Females (13-49 years old)	0.009502	2.1

Adults (20-49 years old)	0.007233	1.6

Adults (50+ years old)	0.008468	1.9

cPAD = chronic  population adjusted dose 

* Exposure estimates based on tolerance values, default processing
factor, and 100% crop treated values 

 

Results of the analysis show that for the U.S. population and all
sub-populations, the exposures are below a level of concern (< 100%
cPAD).  Additional refinements in the chronic dietary risk assessment
(i.e. utilizing anticipated residue values, process factors, percent
crop treated values) would further reduce the estimated exposure values.
   

.  Based on the US Geological Survey National Water Quality Assessment
program (NAWQA) data, the 90th percentile concentration for acute and
chronic surface water is 0.053 ppb.  The drinking water concentrations
were considered the 0.053 ppb surface water value of dicamba from NAWQA
plus the addition of the DCSA residues (i.e. acute drinking water conc =
0.053 ug/L [dicamba] + 10.1 ug/L  [DCSA], chronic drinking water conc. =
0.053 ug/L [dicamba] + 0.75 ug/L [DCSA]; DCSA values from dicamba RED
document, Table 2).

 

Drinking water contributions were assessed based on the maximum
estimated dicamba water concentrations (dicamba + metabolite DCSA), and
water consumption and body weights reported in CSFII, using DEEM-FCID
software.  The acute and chronic estimated water exposure values are
summarized in Tables 3 and 4, respectively.  Minimal exposure of dicamba
occurs through drinking water with < 0.25% the aPAD and < 0.02 cPAD for
all subpopulations.

  

Table 3. 	Results for Dicamba Acute Water Exposure Analysis Considering
the Maximum Estimated Acute Drinking Water Concentration using 

DEEM-FCID 

Population	Water Exposure Estimate	%aPAD

Subgroups	(mg/kg b.w./day)*	 

U.S. Population	0.00053	0.05

All Infants (< 1 year old)	0.002	0.20

Children (1-2 years old)	0.000832	0.08

Children (3-5 years old)	0.00076	0.08

Children (6-12 years old)	0.000529	0.05

Youth (13-19 years old)	0.00043	0.04

Females (13-49 years old)	0.000491	0.05

Adults (20-49 years old)	0.000444	0.04

Adults (50+ years old)	0.000494	0.05

aPAD = acute  population adjusted dose

*Water exposure estimates using acute surface water value of dicamba
(0.053 ug/L based on NAWQA 90th percentile concentration) + DCSA (10.1
ug/L from Table 2 in dicamba RED document)   

   

Table 4. 	Results for Dicamba Chronic Water Exposure Analysis
Considering the Maximum Estimated Chronic Drinking Water Concentration
using DEEM-FCID 

Population	Water Exposure Estimate	%cPAD

Subgroups	(mg/kg b.w./day)	 

U.S. Population	0.000017	0.00

All Infants (< 1 year old)	0.000055	0.01

Children (1-2 years old)	0.000025	0.01

Children (3-5 years old)	0.000024	0.01

Children (6-12 years old)	0.000016	0.00

Youth (13-19 years old)	0.000012	0.00

Females (13-49 years old)	0.000016	0.00

Adults (20-49 years old)	0.000017	0.00

Adults (50+ years old)	0.000016	0.00

cPAD = chronic  population adjusted dose

*Water exposure estimates using acute surface water value of dicamba
(0.053 ug/L based on NAWQA 90th percentile concentration) + DCSA (0.75
ug/L from Table 2 in dicamba RED document)   

Acute Aggregate Exposure and Risk (Food and water)

The aggregate acute risk includes residues of dicamba from food and
water (Table 5). Exposures from residential uses are not included in the
acute aggregate assessment.  The results demonstrate 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.   

Table 5. 	Estimated Acute Aggregate Exposure and Risk of dicamba  

Population Subgroup	aPAD (mg/kg/day)	Food Exposure (mg/kg/day)	Water
Exposure (mg/kg/day)	Total Exposure (mg/kg/day)	% aPAD

U.S. Population	1	0.029757	0.00053	0.030287	3.03

All Infants (< 1 yr old)	1	0.051651	0.00200	0.053651	5.37

Children 1-2 years	1	0.053779	0.000832	0.054611	5.46

Children 3-5 years	1	0.048466	0.00076	0.049226	4.92

Children 6 – 12 years	1	0.035541	0.000529	0.03607	3.61

Youth 13-19 years	1	0.023578	0.00043	0.024008	2.40

Females 13-49 years	1	0.018052	0.000494	0.018546	1.85

Adults 20-49 years	1	0.021483	0.000491	0.021974	2.20

Adults + 50	1	0.015067	0.000444	0.015511	1.55



Short- and Intermediate Term Aggregate Exposure and Risk (food,water,
and residential)

Short-term aggregate risk from dicamba takes into account exposures from
dietary consumption (food and water) and residential exposure from turf
use.  Post application exposure from the turf use is considered
short-term.  The aggregate MOE from food, water, and residential
exposure are 1105 and 1987 for the children 1-2 years old and the US
population, respectively.  These MOE are greater than the target MOE of
100 that indicates there is no safety concern.  The results of the
analysis are shown in Table 6. 

Table 6. 	Estimated Short/Intermediate Term Aggregate Exposure and Risk
of Dicamba  

Population	NOAEL (mg/kg/day)	Target MOE1	Food Exposure (mg/kg/day)	Water
Exposure (mg/kg/day)	Residential Exposure2 (mg/kg/day)	Total Exposure
(mg/kg/day)	MOE3

US	45	100	0.018928	0.000017	0.0037	0.022645	1987

Child 4	45	100	0.026702	0.000024	0.014	0.040726	1105

1 Target MOE is 100.

2 Residential Exposure = Exposure to adult while playing golf.

3 Aggregate MOE = (NOAEL / (Food + Water + Residential Exposure)

4 Short-term residential exposure was calculated for children 3-years of
age, dietary exposure for children   

  3-5 years of age  

 Chronic Aggregate Exposure and Risk (food and water)

The aggregate chronic risk includes residues of dicamba from food and
water (Table 7). Exposures from residential uses are not included in the
chronic aggregate assessment.  The results demonstrate 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. 

  Table 7. 	Estimated Chronic Aggregate Exposure and Risk of dicamba 

Population Subgroup	cPAD (mg/kg/day)	Food Exposure (mg/kg/day)	Water
Exposure (mg/kg/day)	Total Exposure (mg/kg/day)	% cPAD

U.S. Population	0.45	0.011574	0.000017	0.011591	2.58

All Infants (< 1 yr old)	0.45	0.018928	0.000055	0.018983	4.22

Children 1-2 years	0.45	0.029346	0.000025	0.029371	6.53

Children 3-5 years	0.45	0.026702	0.000024	0.026726	5.94

Children 6 – 12 years	0.45	0.018314	0.000016	0.01833	4.07

Youth 13-19 years	0.45	0.011200	0.000012	0.011212	2.49

Females 13-49 years	0.45	0.008468	0.000016	0.008484	1.89

Adults 20-49 years	0.45	0.009502	0.000016	0.009518	2.12

Adults + 50	0.45	0.007233	0.000017	0.00725	1.61



. 

Dicamba is registered for use on residential and recreational turf.  The
following post-application exposure scenarios were evaluated 1) adults
and toddler post-application dermal exposure 2) toddlers’ incidental
ingestion of pesticide residues on lawns form hand-to-mouth transfer, 3)
toddlers’ object-to-mouth transfer from mouthing pesticide-treated
turfgrass, and 4) toddlers’ incidental ingestion of soil from
pesticide-treated residential areas.  The post-application exposure
assessment was based on generic assumptions specified in the Recommended
Revisions to the Residential Standard Operating Procedures and
recommended approaches by an EPA science advisory council.  A dermal
absorption value of 15% was used in the assessment of dicamba.  The
exposure and risk estimates for the residential exposure scenarios are
assessed for the day of application because adults and toddlers could
contact treated turf immediately after application.  All
short-/intermediate term MOE were greater than 100 which indicates that
exposure from all residential scenarios result in exposures below a
level of concern. 

	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.'  

		No Maximum residue levels (MRLs) have been established for dicamba by
the Codex Alimentarius Commision (CODEX).

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