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bromoxynil (Brominal, Buctril) Pesticide Tolerance Petition 12/96

[Federal Register: December 24, 1996 (Volume 61, Number 248)] [Notices]
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ENVIRONMENTAL PROTECTION AGENCY
[PF-681; FRL-5576-8]
Rhone-Poulenc Ag Company; Pesticide Tolerance Petition Filing 
AGENCY: Environmental Protection Agency (EPA). 
ACTION: Notice of filing.
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SUMMARY: This notice announces the filing of a pesticide petition proposing 
the establishment of a regulation for residues of the herbicide bromoxynil 
(3,5-dibromo-4 hydroxybenzonitrile), resulting from the application of its 
octanoic and heptanoic acid esters. The proposal would extend the time-limited 
tolerance in or on the raw agricultural commodity (RAC) cottonseed (transgenic 
BXN varieties only) at 0.04 part per million. This notice includes a summary 
of the petition that was prepared by the petitioner, Rhone-Poulenc Ag Company. 
DATES: Comments, identified by the docket number [PF-681], must be received on 
or before, January 23, 1997. 
ADDRESSES: By mail, submit written comments to Public Response and Program 
Resources Branch, Field Operations Division (7506C), Office of Pesticide 
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 22202. 
Comments and data may also be submitted electronically by sending electronic 
mail (e-mail) to: opp-docket@epamail.epa.gov. 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 
in 5.1 file format or ASCII file format. All comments and data in electronic 
form must be identified by the docket number [PF-681]. Electronic comments on 
this proposed rule may be filed online at many Federal Depository Libraries. 
Additional information on electronic submissions can be found below in this 
document.
Information submitted as comments concerning this document may be claimed 
confidential by marking any part of 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: Robert Taylor Product Manager (PM 25) Rm., 
241, CM #2, 1921 Jefferson Davis Highway, Arlington, VA 703-305- 6224, e-mail: 
Taylor.Robert@epamail.epa.gov. 
SUPPLEMENTARY INFORMATION: EPA has received a pesticide petition (PP) 3F4233 
from Rhone-Poulenc Ag Company, PO Box 12014 T.W. Alexander Drive, Research 
Triangle Park, North Carolina 27709 porposing pursuant to section 408(d) of 
the Federal Food, Drug and Cosmetic Act (FFDCA), 21 U.S.C. section 346a(d), to 
amend CFR part 180 by establishing a tolerance for residues of the herbicide 
bromoxynil (3,5-dibrom-4- hydroxybenxonitrile), resulting from the application 
of its octanoic and heptanoic acid esters in or on the raw agricultural 
commodity cottonseed at 0.04 ppm. The proposed analytical method is a revised 
version of Method 1 in the Pesticide Analytical Manual (PAM), Vol II. 
As required by section 408(d) of the FFDCA, as recently amended by the Food 
Quality Protection Act, Rhone-Poulenc included in the petition a summary of 
the petition and authorization for the summary to be published in the Federal 
Register in a notice of receipt of the petition. The summary represents the 
views of Rhone-Poulenc; EPA is in the process of evaluating the petition. As 
required by section 408(d)(3) EPA is including the summary as a part of this 
notice of filing. EPA has made minor edits to the summary for the purpose of 
clarity.
EPA invites interested persons to submit comments on this notice of filing. 
Comments must bear a notification indicating the document control number [PF-
681]. All written comments filed in response to this petition will be 
availble, in the Public Response and Program Resources Branch, at the address 
given above from 8:30 a.m. to 4 p.m., Monday through Fridy, except legal 
holidays.
A record has been established for this notice under docket numbers [PF-681] 
(including com ents 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 public record is located in Rm. 1132 of the Public 
Response and Program Resources Branch, Field Operations Division (7506C), 
Office of Pesticide Programs, Environmental Protection Agency, Crystal Mall 
#2, 1921 Jefferson Davis Highway, Arlington, VA. 
Electronic comments can be sent directly to EPA at: opp-docket@epamail.epa.gov
Electronic comments must be submitted as ASCII file avoiding the use of 
special characters and any form of encryption. 
The official record for this rulemaking, as well as the public version, as 
described above will be kept in paper form. Accordingly, EPA will transfer all 
comments received electronically into printed, paper form as they are received 
and will place the paper copies in the official rulemaking record which will 
also include all comments submitted directly in writing. The official 
rulemaking record is the paper record maintained at the address in "ADDRESSES" 
at the beginning of this document.
I. Petition Summary
There is an extensive data base supporting the registration of Bromoxynil and 
its esters. This data base is current as the majority of the studies have been 
submitted and accepted under the reregistration process mandated by FIFRA 88. 
The Reregistration Eligibility Document (RED) for Bromoxynil has been 
scheduled by the Agency for early in fiscal year 1997. Included in this data 
submitted were studies which showed the nature and magnitude of Bromoxynil 
residue in ruminants and poultry. Based on these studies the Agency has 
determined that the nature of the residue in ruminants and poultry are 
understood and that any secondary residues from this tolerance occurring in 
the fat, meat, and meat byproducts of cattle, goats, horses, poultry, and 
sheep will be covered by existing tolerances.
The nature of the residue in Transgenic Cotton is considered to be adequately 
understood. The primary Bromoxynil metabolite is 3,5-dibrom- 4-hydroxybenzoic 
acid (DBHA). DBHA is only a major metabolite in/on transgenic cotton treated 
with Bromoxynil. For the purposes of extending the time-limited tolerance, 
only the parent compound should be regulated as in 40 CFR 180.324. This 
interim decision is based on several factors. There will be very minimal risk 
from total residues of the parent compound and the DBHA metabolite in cotton 
seed contributing only about 1/1000th of the total dietary exposure from all 
registered uses of Bromoxynil. The registration of Bromoxynil on Transgenic 
Cotton in 1997 will be limited to 400,000 acres. This represents less than 3% 
of the total cotton acres anticipated to be planted in 1997. The only other 
potential source of dietary exposure from this use would be from cattle fed 
cotton gin trash. Any potental dietary risk from this source would be even 
less than the risk from cottonseed. This is based on again less than 3% of the 
cotton acres being treated with Bromoxynil. It is also based on the fact that 
the majority of the cotton gin trash is disked back into the fields and not 
fed to cattle. Even when the cotton gin trash is fed to cattle it represents 
only a maximum of 30% of the diet.
Adequate methodology is available for enforcement purposes, based upon methods 
for the parent compound. The method involves sample reflux in methanolic KOH, 
partitioning with ether/hexane and analysis by GC. The limit of detection 
(LOD) for this method is 0.02 ppm. The method is a modified version of Method 
I in the Pesticide Analytical Manual (PAM), Vol. II.
A. Toxicological Profile
The following mammalian toxicity studies have been conducted to support the 
tolerance of bromoxynil:
1. Acute Toxicity--Bromoxynil Phenol Technical. A complete battery of acute 
toxicity studies for Bromoxynil Phenol were completed. The acute oral toxicity 
study resulted in a LD50 of 81 mg/kg (males) and a LD50 of 93 mg/kg (females). 
The acute dermal toxicity study in rabbits resulted in a LD50 of >2000 mg/kg 
for both males and females. The acute inhalation study in rats resulted in a 
LC50 of 0.269 mg/L for males and 0.150 for females. The primary eye irritation 
study showed corneal opacity resolved within 3 days, iritis resolved within 4 
days and conjuctival irritation which persisted for 10 days. There was no 
irritation in the Primary dermal irritation study and the dermal sensitization 
study in guinea pigs was negative. Based on the results of these studies 
Bromoxynil Phenol is placed in toxicity Category II.
2. Acute Toxicity--Bromoxynil Octanoate Technical. A complete battery of acute 
toxicity studies for Bromoxynil Octanoate technical were completed. The acute 
oral toxicity study resulted in a LD50 of 400 mg/kg (males) and a LD 50 of 238 
mg/kg (females). The acute dermal toxicity study in rabbits resulted in a LD50 
of 2000 mg/kg for males with abraded skin, 1310 mg/kg for females with intact 
skin and 1660 mg/kg for females with abraded skin. The acute inhalation study 
in rats resulted in a LC50 of 0.81 mg/L for males and 0.72 mg/L for females. 
The primary eye irritation study showed corneal opacity and irritation lasting 
for 24-72 hours. It had cleared by 96 hours. The primary dermal irritation 
study showed erythema for 72 hours and no edema. The dermal sensitization 
study in guinea pigs showed compound to be a positive contact sensitizer in 
modified Draize test. Based on the results of these studies Bromoxynil 
Octanoate is placed in toxicity category II. 
3. Acute Toxicity--Bromoxynil Heptanoate Technical. A complete battery of 
acute toxicity studies for Bromoxynil Heptanoate were completed. The acute 
toxicity study resulted in a LD50 of 362 mg/ kg (males) and a LD50 of 292 
mg/kg (females). The acute dermal toxicity study in rabbits resulted in a LD50 
of >2020 mg/kg. The acute inhalation study in rats resulted in a LC50 of 1.975 
mg/L for males and 1.479 mg/L for females. Based on the results of these 
studies Bromoxynil Heptanoate is placed in toxicity Category II. 
Conclusion: Based on the acute toxicity data cited above and a margin of 
safety between the most conservative acute oral toxicity value and the oral 
RfD of 0.015 mg/kg/day of >9000, Rhone-Poulenc it is concludeds that neither 
Bromoxynil nor its octanoic or heptanoic acide esters pose any acute dietary 
risks.
B. Mutagenicity
1. Mutagenicity--Bromoxynil Phenol Technical. Mutagenicity studies completed 
included an unscheduled DNA synthesis study-rat primary hepatocytes 
(negative); in vitro transformation assay--mouse cells (negative); sister 
chromosomal exchange study--CHO cells (negative); forward mutation study--
mouse lymphoma cells (negative without activation and positive with 
activation); DNA repair test--E. Coli (positive); in vitro chromosomal 
aberration (negative without activation and positive with activation); two 
separate micronucleus assays (both negative); forward mutation-- CHO cells 
(negative); and an Ames Study--Salmonella typhimurium (negative with and 
without activation).
2. Mutagenicity--Bromoxynil Octanoate Technical. Mutagenicity studies 
completed included an Ames Study--Salmonella typhimurin (negative with and 
without activation); micronucleus assay (negative); and an unscheduled DNA 
synthesis--rat primary hepatocytes (negative). 
Conclusion. Based on the data cited above Rhone-Poulenc concludes neither 
Bromoxynil nor its octanoic or heptanoic acid esters are considered to be 
mutagenic.
C. Rat Metabolism
1. Rat Metabolism--Bromoxynil Heptanoate Technical. Similar results were 
obtained when a single low dose (2 mg/kg), a single high dose (20 mg/kg) and a 
low dose (2 mg/kg) administered for 14 consecutive days were fed to rats. 
Bromoxynil Heptanoate is rapidly absorbed and widely distributed in most 
tissues. The highest concentrations were found in the blood, plasma, liver, 
kidney and thyroid. Higher tissue concentrations were found in females than in 
males while excretion was more rapid in males. Most of the radioactivity was 
excreted in the urine. Most of this was in the form of Bromoxynil Phenol. Both 
Bromoxynil Phenol and Bromoxynil Heptanoate were present in the feces. There 
was no significant retention in tissues after 7 days. Bromoxynil Heptanoate 
was essentially metabolized to Bromoxynil Phenol via ester hydrolysis.
2. Rat Metabolism--Bromoxynil Octanoate Technical. The study demonstrated that 
2 mg/kg of radiolabeled Bromoxynil Octanoate was rapidly absorbed, 
distributed, and excreted in rats following repeated oral administration. A 
sex-related difference was seen in the excretion of Bromoxynil Octanoate. The 
urine was the major route of excretion, representing 80.24% of the 
administered dose in males and 67.91% in females at 7 days post-dosing. The 
urinary excretion rate was also higher in males than in females. The feces 
accounted for 7 - 10% of the administered dose at 7 days post-dosing. A sex-
related difference was also noted in tissue bioaccumulation of Bromoxynil 
Octanoate with 1.482% of the dose in males and 8.036% in females. Tissue 
distribution was similar for both sexes with the highest radioactivity 
recovered in the liver and kidney. Bromoxynil Octanoate was essentially 
metabolized to Bromoxynil Phenol via ester hydrolysis. 
D. Chronic Effect:
A 1 year oral dog study was run with dogs administered Bromoxynil Phenol at 
dose levels of 0, 0.1, 0.3, 1.5, and 7.5 mg/kg/day in capsules. The NOEL/LEL 
is 1.5 mg/kg/day for both females and males based on decreased body weight 
gain, decreased RBC count, decreased hemoglobin, decreased PCV, increased 
liver weights. 
Conclusion: The chronic dog study was determined by the EPA to be the most 
appropriate study for setting the RfD of 0.015 mg/kg/day (includes a 100 fold 
safety factor). Based on the chronic toxicity data cited above Rhone-Poulenc 
concludes that neither Bromoxynil nor its octanoic or heptanoic acid esters 
pose any chronic dietary risks. 
E. Carcinogenicity
Several feeding/carcinogenicity studies were conducted with Bromoxynil Phenol. 
These studies are summarized below. 
1. A 2 year combined feeding/carcinogenicity study was conducted with rats 
administered (oral) dosages of 0, 60, 190, or 600 ppm (0, 2.6, 8.2, or 28 
mg/kg/day in males; 0, 3.3, 11.0, or 41 mg/kg/day in females) Bromoxynil 
Phenol in the diet. In males the no-observed- effect-level (NOEL) for systemic 
toxicity is 2.6 mg/kg/day, and the Lowest-effect-level (LEL) is 8.2 mg/kg/day. 
In females, the NOEL is 3.3 mg/kg/day, and the LEL is 11.0 mg/kg/day. This 
study did not demonstrate any increase in tumor incidences in either male or 
female rats.
2. A 2 year combined feeding/carcinogenicity study was conducted with rats 
administered Bromoxynil Phenol in the diet at dose levels of 0, 10, 30, or 100 
ppm (0, 0.5, 1.5, or 5 mg/kg/day). In both males and females, the NOEL and 
LOEL for systemic toxicity was 5 mg/kg/day and >5 mg/kg/day, respectively. At 
the highest dose tested, increased liver weights were observed at 12 months, 
but not at 24 months. This study was considered negative for carcinogenicity. 
3. An 18 month carcinogenicity study was conducted with mice administered 
Bromoxynil Phenol at dose levels of 0, 10, 30, or 100 ppm (0, 1.3, 3.9, or 13 
mg/kg/day) in the diet. For males, dose related increases in hyperplastic 
nodules and liver adenomas/carcinomas were observed which were statistically 
significant at the 13 mg/kg/day level. Increased relative liver weights were 
also observed. In females, increased absolute liver weights and relative liver 
and kidney weights were observed. The study was considered negative for 
carcinogenicity for females.
4. An 18 month carcinogenicity study was conducted with mice administered 
Bromoxynil Phenol at dose levels of 0, 20, 75, or 300 ppm (0, 3.1, 12 or 46 
mg/kg/day in males and 0, 3.7, 14, or 53 mg/kg/day in females). Mice given 300 
ppm had significantly increased absolute and relative liver weights. 
Histopathology of the liver revealed increased hepatocellular hypertrophy, 
hepatocellular degeneration, necrosis of individual hepatocytes, and pigment 
accumulation in hepatocytes and Kupffer cells. Male mice had statistically 
significant increased numbers of hepatocellur adenomas and carcinomas at 20 
ppm, but not 75 ppm. In contrast, no significant increase in tumor incidence 
was observed for female mice by pair-wise analysis. The trend test was 
significant for adenomas or carcinomas in females, only at p<0.05, not p<0.01 
as would be appropriate for this type of tumor. The trend is due entirely to 
the high dose group and therefore is of questionable validity. 
Conclusion. Bromoxynil is a weak, single sex, single species, non- metastic, 
single target organ carcinogen, inducing hepatocellular tumors in male mice 
exposed to 300 ppm for 18 months. These tumors and associated 
histopathological findings are consistent with secondary mechanisms such as 
peroxisome proliferation, a mechanism known to have marked species differences 
and questionable relevance for humans. The data are not suitable for 
quantitative risk assessment. A threshold safety factor approach is more 
appropriate and is commonly used for single sex, single species carcinogens 
such as Bromoxynil that are thought to work through secondary mechanisms. 
Based on these data, Rhone-Poulenc concludes Bromoxynil is not expected to 
pose any increased dietary risks.
F. Teratology
1. Bromoxynil Phenol Technical. Several teratology studies were conducted with 
Bromoxynil Phenol Technical. These are summarized below: 
a. A teratology study was conducted with rats administered (orally) Bromoxynil 
Phenol at dose levels of 0, 4, 12.5, or 40 mg/kg/ day. The maternal NOEL and 
LEL are 12.5 and 40 mg/kg/day respectively. The developmental NOEL and LEL are 
4.0 and 12.5 mg/kg/day, respectively. Maternal body weights and food 
consumption were reduced in the high dose group. Fetal effects observed were 
reduced body weight, with associtaed decreases in ossification. An increase in 
14th ribs, was observed in the mid and high dose levels. 
b. A teratology study was conducted with rats administered (orally) Bromoxynil 
Phenol at dose levels of 0, 5, 15, or 35 mg/kg/day. The maternal NOEL and LEL 
are 5.0 and 15 mg/kg/day, respectively. The fetotoxicity and developmental 
NOEL and LEL are less than 5 and 5 mg/ kg/day, respectively. Significant 
maternal mortality and decreased body weight gain were associated with the 
high dose, indicating that the MTD was exceeded. Decreases in maternal body 
weight gain were also observed in the mid and low dose levels. At the mid-dose 
level a statistically significant increase in the number of fetuses with 
supernumerary ribs, a common fetal variant was observed.
c. A teratology study was conducted with rats administered (orally) Bromoxynil 
Phenol at dose levels of 0, 1.7, 5, or 15 mg/kg/ day. The maternal NOEL and 
LEL sre 5 and 15 mg/kg/day, respectively. The developmental NOEL and LEL are 5 
and 15 mg/kg/day, respectively. This study was classified as unacceptable, 
primarily due to reporting deficiendies.
d. A teratology study was conducted with rabbits administered (orally) 
Bromoxynil Phenol at dose levels of 0, 15, 30, or 60 mg/kg/ day. The maternal 
NOEL and LEL are 15 and 30 mg/kg/day, respectively. The developmental NOEL and 
LEL are less than 15 and 15 mg/kg/day, respectively. Significant body weight 
gain decrements were reported at the two highest dose levels along with 
observed decreases in food sonsumption. The severe maternal toxicity among 
high dose dams was associated with fetoxicity and teratogenicity. A slight, 
nonsignificant increase in supernumerary ribs was reported at the mid and low 
dose levels.
e. A teratology study was conducted with mice administered (orally) Bromoxynil 
Phenol at dose levels of 0, 11, 32, or 96 mg/kg/ day. Maternal mortality was 
observed at 32 and 96 mg/kg/day. Fetal body weight was decreased at the top 
dose level, associated with a decrease in caudal vertebral ossification and an 
increase in supernumerary ribs. The maternal NOEL and LEL are 11 and 32 
mg/kg/day respectivel. The developmental NOEL and LEL are 32 and 96 mg/kg/day, 
respectively. 
2. Bromoxynil Octanoate Technical. A teratology study was conducted with 
Bromoxynil Octanaote administered (orally) to rats at dose levels of 0, 2.4, 
7.3 or 21.8 mg/kg/day. This is equivalent to 0, 1.7, 5, or 15 mg/kg/day 
Bromoxynil Phenol. Transient decreases in maternal body weight were observed 
at the highest dose level. Fetal body weight was also decreased and the 
incidence of supernumerary ribs was increased at this dose level. The maternal 
NOEL and LEL are 5 and 15 mg/kg/day, respectively. The developmental NOEL and 
LEL are also 5 and 15 mg/kg/day, respectively.
Conclusion. Based on all the studies cited above Rhone-Poulenc concludes that 
neither Bromoxynil nor Bromoxynil Octanoate are teratogens at doses that are 
not maternally toxic. 
G. Reproductive Effects
1. Two reproduction studies were conducted with Bromoxynil Phenol. These are 
summarized below:
a. A reproduction study was conducted with rats administered (orally) 
Bromoxynil Phenol at dose levels of 0. 0.8, 4, or 21 mg/kg/day in the diet. 
The systemic adult rat NOEL is 4 mg/kg/day and the LEL is 21 mg/kg/day. The 
reproductive NOEL is 21 mg/kg/day, and the LEL is greater than 21 mg/kg/day. 
The postnatal developmental NOEL is 4 mg/kg/ day, and the LEL is 21 mg/kg/day. 
Body weight gain decrements were reported. However, no adverse effects on 
fertility, fecundity, reproductive performance or pre and postnatal 
development were observed.
b. A reproduction study was conducted with rats administered (orally) 
Bromoxynil Phenol at dose levels of 0, 1.5, 5, or 15 mg/kg/day in the diet. 
The systemic rat NOEL is 1.5 mg/kg/day, and the LEL is is 5 mg/kg/day. The 
reproductive NOEL is 15 mg/kg/day, and the LEL is greater than 15 mg/kg/day. 
The offspring developmental NOEL is 5 mg/kg/ day and the LEL is 15 mg/kg/day. 
Body weight gain decrements were reported. However, no adverse effects on 
fertility, fecundity, reproductive performance or pre and postnatal 
development were observed.
Conclusion. Based on the studies cited above Rhone-Poulenc concludes 
Bromoxynil is not considered a reproductive toxicant and shows no evidence of 
endocrine effects.
2. Aggregate Exposure. The Food Quality Protection Act of 1996 list three 
other potential sources of exposure to the general population that must be 
addressed. These are pesticides in drinking water, exposure from non-
occupational sources, and the potential cumulative effect of pesticides with 
similar toxicological modes of action. Based on available studies which show a 
short half-life of Bromoxynil in the environment (average half-life of 3-7 
days under actual field conditions), Rhone-Poulenc does not anticipate 
residues of Bromoxynil in drinking water. There is no established Maximum 
Concentration Level or Health Advisory Level for Bromoxynil under the Safe 
Drinking Water Act.
The potential for non-occupational exposure to the general public is also 
insignificant. There are no residential lawn or garden uses for Bromoxynil 
products where the general population may be exposed via inhalation or dermal 
routes. Bromoxynil is registered for use on grass grown for seed or sod 
production and for non-residential turfgrass. These uses are very minor and 
applied at only 0.5 lbs per acre. These uses will therefore not significantly 
add to the aggregate exposure. 
Rhone-Poulenc concludes that consideration of a common mechanism of toxicity 
is not appropriate at this time since there is no reliable data to indicate 
that the toxic effects caused by Bromoxynil would be cumulative with those of 
any other compound. Based on this point, Rhone-Poulenc has considered only the 
potential risks of Bromoxynil in its exposure assessment.
C. Safety Determination
1. DRES-U.S. Population, Infants, Children (1-6 years old) a. General U.S. 
population. Using the stated EPA RfD for bromoxynil of 0.015 mg/kg/day and the 
conservative assumptions stated above, and based on the completeness of the 
toxicology database, it has been determined that aggregate exposure to 
Bromoxynil will use 2.4% of the RfD for the US population. This is assuming 
that 100% of the acres for each crop for which a tolerance has been 
established (including transgenic cotton) was treated and the residue found 
was at the tolerance level. If one assumes market share values this number is 
decreased to 1.4%.
b. Infants and children (1-6 years old). The Food Quality Protection Act of 
1996 provides that an additional safety factor for infants and children may be 
applied in the case of threshold effects. The NOEL/LEL of 1.5 mg/kg/day in the 
chronic dog study, on which the RfD is based, is already lower than the NOELs 
from the developmental and reproductive toxicity studies. Rhone-Poulenc 
concludes that an adequate margin of safety is therefore provided by the 
currents RfD. Using the stated EPA RfD for Bromoxynil of 0.015 mg/kg/day and 
the conservative assumptions stated above, it has been determined that 
aggregate exposure to Bromoxynil will use 2.3% for infants and 4.9% for 
children under 6 years old. This is assuming that 100% of the acres for each 
crop for which a tolerance has been established (including transgenic cotton) 
was treated and the residue found was at the tolerance level. If one assumes 
market share values these values are decreased to 1.8% for infants and 2.8% 
for children under 6 years old. 
c. Additional Comments on Safety to Infants and Children. In assessing the 
potential for additional sensitivity of infants and children to residues of 
Bromoxynil, the available teratology and reproductive toxicity studies and the 
potential for endocrine modulation by Bromoxynil were considered. 
Developmental toxicity studies in three species indicates that Bromoxynil is 
not a teratogen at doses that are not maternally toxic. Two multi-generation 
rodent reproduction studies demonstrated that there were no adverse effects on 
reproductive performance, fertility, fecundity, pup survival, or pup 
development. Maternal and developmental NOELs and LOELs were comparable 
indicating no increase susceptibility of developing organisms. No evidence of 
endocrine effects were noted in any study. Rhone-Poulence concludesIt is 
therefore concluded that Bromoxynil poses no additional risk for infants and 
children and no additional uncertainty factor is warrented.
d. Environmental Fate. Extensive laboratory and field studies indicate that 
bromoxynil has little tendency to move within or persist in soil or water 
under field conditions. Once in contact with soil, bromoxynil rapidly 
degrades. An average half-life of 3-7 days for bromoxynil has been 
demonstrated under field conditions. The soil breakdown process begins almost 
immediately and involves hydrolysis, dehalogenation, as well as other complex 
metabolic pathways carried out by soil bacteria and other microorganisms. 
II. Administrative Matters
Interested persons are invited to submit comments on this notice of filing. 
Comments must bear a notation indicating the document control number, [PF-
681]. All written comments filed in response to this petition will be 
available in the Public Response and Program Resources Branch, at the address 
given above from 8:30 a.m. to 4 p.m., Monday through Friday, except legal 
holidays.
A record has been established for this notice of filing under docket number 
[PF-681] 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, 
except legal holidays. The public record is located in Rm. 1132 of the Public 
Response and Program resources Branch, Field Operations Division (7506C), 
Office of Pesticide Programs, Environmental Protection Agency, Crystal Mall 
#2, 1921 Jefferson Davis highway, Arlington, VA. 
Electronic comments can be sent directly to EPA at: opp-docket@epamail.epa.gov
Electronic comments must be submitted as an ASCII file avoiding the use of 
special characters and any form of encryption. 
The official record for this notice of filing, as well as the public version, 
as described above will be kept in paper form. Accordingly, EPA will transfer 
all comments received electronically into printed, paper form they are 
received and will place the paper copies in the official record which will 
also include all comments submitted directly in writing. The official 
rulemaking record is the paper record maintained at the address in "ADDRESSES" 
at the beginning of this document.
List of Subjects
Environmental Protection, Administrative practice and procedure, Agricultural 
commodities, Pesticide and pest, Reporting and recordkeeping requirements.
Dated: December 13, 1996.
Peter Caulkins,
Acting Director, Registration Division, Office of Pesticide Programs. 
[FR Doc. 96-32530 Filed 12-23-96; 8:45 am]