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Fluazifop-butyl. TOXNET profile from Hazardous Substances Data Bank.
See for Updates: http://toxnet.nlm.nih.gov/cgi-bin/sis/search
FLUAZIFOP-BUTYL
CASRN: 69806-50-4
For other data, click on the Table of Contents
Human Health Effects:
Emergency Medical Treatment:
Animal Toxicity Studies:
Non-Human Toxicity Excerpts:
Very low toxicity to bees, both orally and by contact.
Low toxicity to aquatic invertebrates.
Mild skin and eye irritant; practically non-irritating to eyes (rabbits).
Not a skin sensitizer (guinea pigs).
Non-Human Toxicity Values:
LD50 Rat male oral >2,000 mg/kg, female rat 3,600 mg/kg
LD50 male Mouse male oral 1,490 mg/kg, female mouse 1,770 mg/kg
LD50 Guinea pig male oral 2,659 mg/kg
LD50 Rabbit oral 621 mg/kg
LD50 Rat percutaneous >6,050 mg/kg
LD50 Rabbit percutaneous >2,420 mg/kg
LC50 Rat inhalation >5.24 mg/L/4 hr
LD50 Rat ip 1,761 mg/kg
NOEL Dog 5 mg/kg daily /1 yr feeding trial/
NOEL Rat 100 mg/kg diet /90-day feeding trial/
NOEL Mouse 5 mg/kg diet /2-yr feeding trial/
LD50 Rat oral 3,328 mg/kg
Ecotoxicity Values:
LD50 Mallard duck oral >17,000 mg/kg
LC50 Mallard duck >25,000 mg/kg diet/5-Day dietary/
LC50 Ring-necked pheasants >18,500 mg/kg diet /5-Day dietary/
LC50 Rainbow trout 1.37 mg/L/96 hr /conditions of bioassay not specified/
LC50 Mirror carp 1.31 mg/L/96 hr /conditions of bioassay not specified/
LC50 Bluegill sunfish 0.53 mg/L/96 hr /conditions of bioassay not specified/
TSCA Test Submissions:
Fluazifop-butyl (CAS # 69806-50-4)
was evaluated for subchronic oral toxicity in beagle dogs (4/sex/group) administered
doses of 0 (vehicle control, corn oil), 5, 25 and 250 mg/kg/day in gelatin capsules
for 13 weeks. Severe corneal ulceration, requiring humane sacrifice of 2 males
and 1 female of a 250 mg/kg/day dosage during Week 4, prompted adjustment of
this regimen to 125 mg/kg/day for the remainder of study. Prior to sacrifice,
these dogs also exhibited progressive conjunctivitis and photophobia, and all
lost weight. Hematology revealed reduced platelet counts, neutrophilia and immature
white cells. Bilirubin, and alanine amine-transferase and alkaline phosphatase
activity were elevated, and plasma protein concentrations were slightly depressed.
The urine contained bile pigments and appeared bright yellow. Distended gall
bladders, large friable livers and congested caecum and colon from engorgement
of the blood vessels were noted upon necropsy. Histopathological evaluation
confirmed treatment-related lesions of the eyes, liver, testes and gastrointestinal
tract. Conversely, all dogs surviving 13-week treatment showed no clinical signs
of toxicity, and no treatment-related changes on physical and ophthalmic examinations
at Weeks 4, 8 and 12. All observed abnormalities were noted solely in the high-dose
treatment group, including reduced food intake and bodyweight gains were most
pronounced from Weeks 4-8 and reduced platelet counts, as seen in the early
sacrificed animals, were resolved upon reduction of the dosage. Alkaline phosphatase,
alanine amino-transferase and aspartate amino-transferase activities were increased
in 250 mg/kg/day males just prior to the adjustment to a 125 mg/kg/day dosage,
while both high-dose females and males exhibited alanine amino-transferase activity
throughout 13-week treatment. High-dose dogs also had increased bromosulphonphthalein
retention at the end of treatment, while glucose and cholesterol were slightly
reduced throughout study. Upon terminal necropsy, organ weights and gross pathology
of dogs surviving 13-week study were unremarkable and histopathological analysis
identified a solitary incidence of arrested maturation in the testicular germinal
epithelium of one high-dose male.
Fluazifop-butyl (CAS # 69806-50-4)
was evaluated for subchronic dietary toxicity in Wistar rats (20/sex/group)
receiving 0, 10, 100 and 2000 ppm by dietary inclusion for 13 weeks. Mean achieved
dosages during 13-week treatment were 0, 0.7, 7.1 and 144.5 mg/kg/day in males
of the respective treatment groups and 0, 0.8, 8.0 and 161.9 mg/kg/day in females.
No mortality or pharmacotoxic signs were documented throughout treatment at
any exposure level. In males of a 2000 ppm dietary exposure, treatment was associated
with depressed food intake and bodyweight gains. Less efficient food utilization
was noted in the high-dose males relative to controls. High-dose males also
exhibited abnormalities in hematological values (Weeks 5 and 11), including
slightly depressed packed cell volume, hemoglobin concentration and red blood
cell count. The serum chemistry in this group was characterized by elevated
alkaline phosphatase values, and higher alanine amino-transferase and aspartate
amino-transferase activities. Also, cholesterol and total protein concentrations
were low as compared to controls. The plasma of 2000 ppm females was found at
Week 11 with depressed total protein and albumin contents relative to controls.
Again at Week 11, isolated instances of elevated urinary protein levels were
identified among high-dose males and females. Upon terminal necropsy, only high-dose
males had evidence of hepatic enlargement or swelling (7/20), although higher
absolute and relative liver weights were significant (p < 0.01, Student's
t-test) in both males and females of the 2000 ppm group. Also, relative kidney
weights were also significantly elevated in the high-dose males. Histopathology
confirmed a specific liver toxicity in male rats, marked by significant dose-related
hepatocytic hypertrophy with isolated instances of vesicular nuclei and or periacinal
hepatocytic necrosis. Renal tubular degeneration, 70% and 20% in 2000 and 100
ppm males respectively, correlated with elevated kidney weights in these groups.
Fluazifop-butyl (CAS # 69806-50-4)
was evaluated for subacute oral toxicity in Wistar albino rats (10/sex/group)
administered 10 ml/kg doses in corn oil of 0, 4, 20, 100 and 500 mg/kg/day by
oral gavage, 5 days/week for 2 weeks. Five-day weekly treatment periods were
each followed by 2-day recovery. High-dose males only displayed overt toxicity
and comprised the 2 study lethalities. These two 500 mg/kg/day males were sacrificed
in extremis on Days 11 and 14 with severe pharmacotoxic signs including piloerection,
reduced motor activity, retinal pallor, and a prone or hunched posture. One
rat was bleeding from the penis. High-dose males consumed less food than control
rats and their growth rate was depressed from Day 10, although mean bodyweights
by the end of study were not significantly lower than controls. Hematology and
serum chemistries suggested a primary toxicity of the liver, mostly in high-dose
males. Males of the 500 mg/kg/day dosage group were found with statistically
significant deficiencies in group mean hemoglobin concentration, packed cell
volume, mean cell volume and erythrocyte count. Also, neutrophil counts were
elevated and activated thromboplastin times were also increased in a dose-related
manner. Blood chemistry indicated a dose-related elevation of alkaline phosphatase
activity in 100 and 500 mg/kg/day males, elevated aspartate amino-transferase
activity in 500 mg/kg/day males, and elevated cholesterol concentrations in
500 mg/kg/day males and females. Conversely, enzyme activity was depressed in
rats of lower dosages. Blood samples from 1 rat killed in extremis showed still
greater stimulation of enzyme activity, with reduced plasma proteins and electrolyte
imbalance. Bone marrow cytology was negative for any treatment-related changes.
Upon gross necropsy, no gross lesions related to treatment were identified.
The decedent animals were found with abnormal upper gastrointestinal contents,
and one rat exhibited congestion of mesenteric lymph nodes with pallor of kidneys,
liver and spleen. Male rats of 100 and 500 mg/kg/day dosages had higher absolute
and relative liver weights that was not seen in their female counterparts. Microscopic
examination confirmed a particular liver pathology of treated males, characterized
by dosage-related hepatocytic hypertrophy and necrosis (study lethalities),
and dosage-related slight to moderate periacinal hepatocytic hypertrophy. Females
of the 2 highest dosage groups only demonstrated dosage-related, slight increases
in periacinal hypertrophy. Micropathological changes also included decreased
periacinal hepatocytic anoxic vacuolation in all males but those of the highest
dosage group and a universal treatment-related extramedullary hemopoiesis.
Fluazifop butyl (CAS # 69806-50-4)
was evaluated for developmental toxicity in the progeny of Sprague-Dawley CD
rats administered oral doses of 0 (corn oil vehicle control), 10, 50 and 200
mg/kg/day by gavage on gestation days 6-20. The general condition of treated
rats was comparable to controls. Treatment did not alter food consumption and
usage efficiency, although terminal mean bodyweights were significantly (p <
0.05; multiple t-test) depressed in the high-dose (200 mg/kg/day) group. Gravid
uterus weights were also significantly (p < 0.01) elevated in association
with the high dosage. Relative liver weights were also significantly (p <
0.05) greater in high-dose dams. Upon necropsy, no in-utero fetal mortality
was attributable to treatment. Delayed fetal ossification and reduced fetal
weight were dose-related and evident at all treatment levels, although fetal
weights in association with dosages of 10 and 50 mg/kg/day were within the threshold
of historical controls. Observed low incidence diaphragmatic hernia in fetuses
of treated animals was also presumed a toxic response, although an unequivocal
dose-response relationship was not established.
Fluazifop butyl was evaluated for
reproductive and developmental effects in 2 successive generations of Charles
River Wistar strain rats (30/sex/group) exposed continuously to 0, 10, 80 and
250 ppm in the diet. Each respective parent generation had received treatment
for a minimum of 100 days (F0) and 120 days (F1) prior to mating. F0 and F1
dams weaned their progeny for 25 days postpartum to time of offspring selection
for mating and continued study (F1) or sacrifice (F1, F2). Thirty days after
sacrifice of their offspring, the surviving F1 females and select F1 males were
sacrificed and with representative F1 and F2 offspring were examined histologically.
The reproductive organs of remaining F0 and F1 males were likewise investigated
for micropathological signs of toxicity. Treatment in the F0 generation could
not be credited with any mortality or clinical toxicity, despite confirmation
of effective serial dosing by metabolite determinations in the urine of treated
animals. While males of all F1 treatment groups also showed no evident response
to treatment, F1 female bodyweight gains were significantly (p < 0.01; multiple
t-test) inflated during maturation in association with a 250 ppm dietary exposure
and significantly depressed during gestation in association with 80 and 250
ppm exposures. No significant treatment-related effects were noted during the
lactation period in either F0 or F1 females. Food consumption, conversion efficiency,
and water intake were unremarkable at all treatment levels in both generations
of treated male and female rats. In both F0 and F1 dams exposed to dietary levels
up to 250 ppm, the gestrous cycles, pre-coital interval, mating, pregnancy,
fertility and gestation indices were unaffected by treatment. Reproductive effects
common to both generations included a significantly extended gestation period
(80, 250 ppm) and significantly reduced litter sizes at postpartum Day 1 (250
ppm). There was a slight dosage-related decrease in implantation scars noted
on necropsy of F0 dams, however viability, bodyweight at postpartum Day 1, bodyweight
gain, sex ratio, auditory and visual function, and all physical development
parameters of the F1 offspring were comparable to controls. Upon necropsy, these
F1 progeny were found with dose-related increased hydronephrosis. Bone marrow
smears and absolute and relative organ weights did not indicate an untoward
effects of treatment, however micropathological investigation identified increased
focal nephrocalcinosis in female F1 offspring of 80 and 250 ppm parents and
male offspring of the 250 ppm parents. Necropsy of F0 parents revealed no gross
pathology and, although testes and epididymis of F0 males of a 250 ppm exposure
were reduced, histological review identified no treatment-related changes. Conversely,
F1 parents were found with gross indications of toxicity. Liver and kidney weights
were significantly high (250 ppm) relative to controls, while spleen weights
were low in both sexes (80, 250 ppm). Testis and epididymis weights in the males
(80, 250 ppm), and pituitary gland (80, 250 ppm), uterus (80, 250 ppm), brain
(250 ppm) and lung weights (250 ppm) in females
were significantly reduced. Female F1 ovarian
weights were increased relative to controls in association with a 250 ppm dietary
exposure. Upon histological investigation, increased incidence geriatric nephropathy
(both sexes, 80 and 250 ppm), distension of mesenteric and/or cervical lymph
nodes (250 ppm) and increased severity of nephrocalcinosis (females, 80 and
250 ppm), and an increased slight testicular tubular atrophy in males (250 ppm)
were noted. F2 female progeny of 250 ppm exposed parents were found with significantly
increased absolute and relative spleen weights. Histological changes were limited
to marginal increases in hydronephrosis.
Fluazifop butyl was evaluated for
developmental toxicity in adult virgin Sprague-Dawley CD rats (160/group) administered
oral doses of 0, 1, 5, 10 and 200 mg/kg/day during gestation days 6-20. No increased
maternal mortality or overt toxicity was attributed to treatment. At gestation
Day 21 sacrifice of the dams, a slight but significantly depressed mean bodyweight
gain among those of a 200 mg/kg/day dosage was indicative of dose-related and
significant (p < 0.05; Student's t-test) reduction in gravid uterus weights.
Significant (p < 0.01; Student's t-tests) dosage-related reductions in fetal
weights in association with treatment from 5 mg/kg/day were found to correlate
with increased incidence of small fetuses. Also, placental weights were also
significantly low in association with treatment at 200 mg/kg/day relative to
controls. Gross pathological changes included increased incidence of diaphragmatic
hernia (4.4% in association with 200 mg/kg/day) noted at all treatment levels
relative to controls (0%), and slight dosage-related increased occurrence of
hydroureter, partnered with a marginal increase in hydronephrosis in 200 mg/kg/day
fetuses. Micropathological investigation validated dosage-related incidence
of hydroureter, hydronephrosis in association with a 200 mg/kg/day regimen,
and subcutaneous edema among 200 mg/kg/day fetuses. Skeletal
examinations further revealed retarded ossification that was dosage-related
in fetuses of gestational treatment levels of 5 mg/kg/day and above. Treatment
levels of 1 mg/kg/day were associated with no toxic, reproductive or developmental
consequences relative to controls under the conditions of this study.
Metabolism/Pharmacokinetics:
Metabolism/Metabolites:
In plants, fluazifop-butyl is rapidly
hydrolyzed to fluazifop.
Mechanism of Action:
Acts by interfering with ATP production.
Pharmacology:
Environmental Fate & Exposure:
Environmental Fate/Exposure Summary:
Fluazifop-butyl will have been released
to the environment from its former use a highly selective post-emergence grass
killer. If released to the atmosphere, fluazifop-butyl's
measured vapor pressure of 4.1X10-7 mm Hg at 20 deg C indicates that it will
exist in both the vapor and particulate phases in the ambient atmosphere. Vapor-phase
fluazifop-butyl will be rapidly degraded
in the atmosphere by reaction with photochemically-produced hydroxyl radicals;
the half-life for this reaction in air is estimated to be 13 hours. Particulate-phase
fluazifop-butyl may be physically removed
from the atmosphere by wet and dry deposition. If released to soil, an estimated
Koc of 6700 indicates that fluazifop-butyl
will be immobile. Fluazifop-butyl has
been found to bind strongly with homoionic clays. Volatilization from wet and
dry soil surfaces is not expected to be an important process given this compound's
estimated Henry's Law constant of 2.1X10-7 atm-cu m/mole and its measured vapor
pressure, respectively. Biodegradation is expected to be an important fate process
for fluazifop-butyl, especially in moist
soils. A half-life of less than one week was observed in moist soils, the major
degradation product being fluazifop.
If released into water, this compound is expected to adsorb strongly to suspended
solids and sediment in the water column based on its estimated Koc. Volatilization
from water surfaces is not expected to be an important fate process based on
the estimated Henry's Law constant for this compound. The potential for bioconcentration
in aquatic organisms is very high based on an estimated BCF of 1500. Hydrolysis
half-lives of 2.2 years and 79 days have been estimated for fluazifop-butyl
at pHs 7 and 8, respectively. Abiotic hydrolysis of fluazifop-butyl
has been observed to be catalyzed by soil colloids. (SRC)
Artificial Pollution Sources:
Fluazifop-butyl's former use as a
highly selective post-emergence grass killer(1) will have resulted in its release
to the environment(SRC).
Environmental Fate:
TERRESTRIAL FATE: Based on a recommended classification scheme(1), an estimated
Koc value of 6700(SRC), determined from a measured log Kow of 4.5(2) and a recommended
regression-derived equation(3), indicates that fluazifop-butyl
is expected to be immobile in soil(SRC). Volatilization of fluazifop-butyl
from moist and dry soil surfaces is not expected to be important(SRC) given
an estimated Henry's Law constant of 2.1X10-7 atm-cu m/mole(SRC), from its experimental
values for vapor pressure, 4.1X10-7 mm Hg(2), and water solubility, 1 mg/l(2),
and this compound's vapor pressure(2), respectively. Biodegradation of fluazifop-butyl
in soil is expected to be important(SRC); fluazifop-butyl
is rapidly biodegraded in moist soils, with a half-life of less than 1 week;
the major degradation product being fluazifop(4).
AQUATIC FATE: Based on a recommended classification scheme(1), an estimated
Koc value of 6700(SRC), determined from a measured log Kow of 4.5(2) and a recommended
regression-derived equation(3), indicates that fluazifop-butyl
is expected to adsorb to suspended solids and sediment in water(SRC). Volatilization
from water surfaces is not expected to be an important process(3,SRC) based
on an estimated Henry's Law constant of 2.1X10-7 atm-cu m/mole(SRC) from its
experimental values for vapor pressure, 4.1X10-7 mm Hg(2), and water solubility,
1 mg/l(2). According to a classification scheme(5), an estimated BCF of 1500(3,SRC),
from a measured log Kow(2), suggests that bioconcentration in aquatic organisms
is very high(SRC). Biodegradation of fluazifop-butyl
in aquatic systems may be important(SRC), given its microbial degradation in
moist soils(6). Hydrolysis half-lives of 2.2 years and 79 days have been estimated
for fluazifop-butyl at pHs 7 and 8,
respectively(7).
ATMOSPHERIC FATE: According to a model of gas/particle partitioning of semivolatile
organic compounds in the atmosphere(1), fluazifop-butyl,
which has a measured vapor pressure of 4.1X10-7 mm Hg at 20 deg C(2), will exist
in both the vapor and particulate phases in the ambient atmosphere. Vapor-phase
fluazifop-butyl is degraded in the atmosphere
by reaction with photochemically-produced hydroxyl radicals(SRC); the half-life
for this reaction in air is estimated to be about 13 hours(3,SRC). Particulate-phase
fluazifop-butyl may be physically removed
from the air by wet and dry deposition(SRC).
Environmental Biodegradation:
Fluazifop-butyl is rapidly biodegraded
in moist soils, with a half-life of less than 1 week, the major degradation
product being fluazifop(1). Conditions
that promote microbial activity in soil, such as high moisture levels have been
found to favor the degradation of fluazifop-butyl
in soil(2). Fluazifop-butyl was rapidly
hydrolyzed by a mixed culture enriched from a landfill leachate to fluazifop(3).
Environmental Abiotic Degradation:
The rate constant for the vapor-phase reaction of fluazifop-butyl
with photochemically-produced hydroxyl radicals has been estimated as 3.0X10-11
cu cm/molecule-sec at 25 deg C(SRC) using a structure estimation method(1,SRC).
This corresponds to an atmospheric half-life of about 13 hours at an atmospheric
concentration of 5X10+5 hydroxyl radicals per cu cm(1,SRC). A base-catalyzed
second order rate constant of 0.10 L/mol-sec(SRC) was estimated using a structure
estimation method(2); this corresponds to half-lives of 2.2 years and 79 days
at pH values of 7 and 8, respectively(2,SRC). Abiotic hydrolysis of fluazifop-butyl
has been observed to be catalyzed by soil colloids(3). Fluazifop-butyl
is resistant to decomposition by ultraviolet radiation(4). Fluazifop-butyl
was rapidly degraded in moist soils (65% and 100% of their field capacity moisture
levels); less than 8% was recoverable after 48 hours(5). In air-dry soils (20%
of field capacity moisture levels), over 90% of fluazifop-butyl
was recovered after 24 and 48 hours(5).
Environmental Bioconcentration:
An estimated BCF of 1500 was calculated for fluazifop-butyl(SRC),
using a measured log Kow of 4.5(1) and a recommended regression-derived equation(2).
According to a classification scheme(3), this BCF suggests that bioconcentration
in aquatic organisms is very high(SRC).
Soil Adsorption/Mobility:
The Koc of fluazifop-butyl is estimated
as approximately 6700(SRC), using a measured log Kow of 4.5(1) and a regression-derived
equation(2,SRC). According to a recommended classification scheme(3), this estimated
Koc value suggests that fluazifop-butyl
is expected to be immobile in soil(SRC). Fluazifop-butyl
is of low mobility in soil(4). Fluazifop-butyl
has been found to bind strongly with homoionic clays(5).
Volatilization from Water/Soil:
The Henry's Law constant for fluazifop-butyl
is estimated as 2.1X10-7 atm-cu m/mole(SRC) from its experimental values for
vapor pressure, 4.1X10-7 mm Hg(1), and water solubility, 1 mg/l(1). This value
indicates that volatilization of fluazifop-butyl
from water surfaces is not expected to be an important fate process(2,SRC).
Fluazifop-butyl's estimated Henry's
Law constant(1,SRC) and measured vapor pressure of 4.1X10-7 mm Hg(1) indicate
that volatilization from moist and dry soil surfaces, respectively, is not expected
to be an important fate process(SRC).
Plant Concentrations:
Residues in potatoes and soybeans treated with fluazifop-butyl
(Fusilade) were below 0.05 ug/g when harvested 90 days after herbicide application(1).
Environmental Standards & Regulations:
FIFRA Requirements:
Tolerances are established for residues for the herbicide fluazifop-butyl(+
or -)-2-(4-(5-(trifluoromethyl)-2-pyridinyl)oxy)phenoxy propanoic acid (fluazifop),
both free and conjugated and of (+ or -)-2-(4-(-(trifluoromethyl)-2-pyridinyl)oxy)phenoxy
propanoate (fluazifop-butyl), all expressed
as fluazifop, in or on the following
raw agricultural commodities: cattle, fat; cattle, meat; cattle, mbyp; cottonseed;
eggs; goats, fat; goats, meat; goats, mbyp; hogs, fat; hogs, meat; hogs, mbyp;
horses, fat; horses, meat; horses mbyp; milk; poultry, fat; poultry, meat; poultry,
mbyp; sheep, fat; sheep, meat; sheep, mbyp; and soybeans.
Tolerances with regional registration are established for residues fluazifop-butyl(+
or -)-2-(4-(5-(trifluoromethyl)-2-pyridinyl)oxy)phenoxy propanoic acid (fluazifop),
both free and conjugated and of (+ or -)butyl-2-(4-(5-(trifluoromethyl)-2-pyridinyl)oxy)phenoxy
propanoate (fluazifop-butyl), all expressed
as fluazifop, in or on the following
raw agricultural commodities: peppers, tabasco.
Tolerances are established for residues of the resolved isomer of fluazifop,
(R)-2-(4-((5-(trifluoromethyl)-2-pyridinyl)oxy)phenoxy)propanoic acid both free
and conjugated and of fluazifop-P-butyl,
butyl(R)-2-(4-((5-(triflluoromethyl)-2-pyridinyl)phenoxy)propanoate, all expressed
as fluazifop, in or on the raw agricultural
commodity: carrots ; endive; macadamia nuts; onions (bulb); pecans; spinach;
stone fruits; and sweet potatoes.
Tolerances with regional registration ... are established for residues of
the resolved isomer of the herbicide fluazifop,
(R)-2-(4-((5-trifluoromethyl)-2-pyridinyl)-oxy)phenoxy)propanoic acid, both
free and conjugated and of fluazifop-P-butyl,
butyl(R)-2-(4-((5-(trifluoromethyl)-2-pyridinyl)oxy)phenoxy)propanoate, all
expressed as fluazifop, in or on the
raw agricultural commodities: asparagus; coffee; and rhubarb.
As the federal pesticide law FIFRA directs, EPA is conducting a comprehensive
review of older pesticides to consider their health and environmental effects
and make decisions about their future use. Under this pesticide reregistration
program, EPA examines health and safety data for pesticide active ingredients
initially registered before November 1, 1984, and determines whether they are
eligible for reregistration. In addition, all pesticides must meet the new safety
standard of the Food Quality Protection Act of 1996. Pesticides for which EPA
had not issued Registration Standards prior to the effective date of FIFRA,
as amended in 1988, were divided into three lists based upon their potential
for human exposure and other factors, with List B containing pesticides of greater
concern and List D pesticides of less concern. Butyl (RS)-2-(4-((5-(trifluoromethyl)-2-pyridinyl)oxy)phenoxy)propanoate
is found on List B. Case No: 2285; Pesticide type: herbicide; Case Status: No
products containing the pesticide are actively registered ... The case /is characterized/
as "cancelled." Under FIFRA, pesticide producers may voluntarily cancel their
registered products. EPA also may cancel pesticide registrations if registrants
fail to pay required fees or make/meet certain reregistration commitments, or
if EPA reaches findings of unreasonable adverse effects.; Active ingredient
(AI): Butyl (RS)-2-(4-((5-(trifluoromethyl)-2-pyridinyl)oxy)phenoxy)propanoate;
Data Call-in (DCI) Date(s): 06/12/91; AI Status: The active ingredient is no
longer contained in any registered pesticide products ... "cancelled.".
Allowable Tolerances:
Tolerances are established for residues for the herbicide fluazifop-butyl(+
or -)-2-(4-(5-(trifluoromethyl)-2-pyridinyl)oxy)phenoxy propanoic acid (fluazifop),
both free and conjugated and of (+ or -)-2-(4-(-(trifluoromethyl)-2-pyridinyl)oxy)phenoxy
propanoate (fluazifop-butyl), all expressed
as fluazifop, in or on the following
raw agricultural commodities: cattle, fat 0.05 ppm; cattle, meat 0.05 ppm; cattle,
mbyp 0.05 ppm; cottonseed 0.1 ppm; eggs 0.05 ppm; goats, fat 0.05 ppm; goats,
meat 0.05 ppm; goats, mbyp 0.05 ppm; hogs, fat 0.05 ppm; hogs, meat 0.05 ppm;
hogs, mbyp 0.05 ppm; horses, fat 0.05 ppm; horses, meat 0.05 ppm; horses mbyp
0.05 ppm; milk 0.05 ppm; poultry, fat 0.05 ppm; poultry, meat 0.05 ppm; poultry,
mbyp 0.05 ppm; sheep, fat 0.05 ppm; sheep, meat 0.05 ppm; sheep, mbyp 0.05 ppm;
and soybeans 1.0 ppm.
Tolerances with regional registration are established for residues fluazifop-butyl(+
or -)-2-(4-(5-(trifluoromethyl)-2-pyridinyl)oxy)phenoxy propanoic acid (fluazifop),
both free and conjugated and of (+ or -)butyl-2-(4-(5-(trifluoromethyl)-2-pyridinyl)oxy)phenoxy
propanoate (fluazifop-butyl), all expressed
as fluazifop, in or on the following
raw agricultural commodities: peppers, tabasco 1.0 ppm.
Tolerances are established for residues of the resolved isomer of fluazifop,
(R)-2-(4-((5-(trifluoromethyl)-2-pyridinyl)oxy)phenoxy)propanoic acid both free
and conjugated and of fluazifop-P-butyl,
butyl(R)-2-(4-((5-(triflluoromethyl)-2-pyridinyl)phenoxy)propanoate, all expressed
as fluazifop, in or on the raw agricultural
commodity: carrots 2.0 ppm; endive 6.0 ppm; macadamia nuts 0.1 ppm; onions (bulb)
0.5 ppm; pecans 0.05 ppm; spinach 6.0 ppm; stone fruits 0.05 ppm; and sweet
potatoes 0.5 ppm.
Tolerances with regional registration ... are established for residues of
the resolved isomer of the herbicide fluazifop,
(R)-2-(4-((5-trifluoromethyl)-2-pyridinyl)-oxy)phenoxy)propanoic acid, both
free and conjugated and of fluazifop-P-butyl,
butyl(R)-2-(4-((5-(trifluoromethyl)-2-pyridinyl)oxy)phenoxy)propanoate, all
expressed as fluazifop, in or on the
raw agricultural commodities: asparagus 3.0 ppm; coffee 0.1 ppm; and rhubarb
0.5 ppm.
Chemical/Physical Properties:
Molecular Formula:
C19-H20-F3-N-O4
Molecular Weight:
383.4
Color/Form:
Pale straw-colored liquid.
Odor:
Odorless
Boiling Point:
165 deg C at 0.02 mm Hg
Melting Point:
13 deg C
Density/Specific Gravity:
1.21 g/cu cm at 20 deg C
Octanol/Water Partition Coefficient:
Log Kow = 4.5
Solubilities:
In water, 1 mg/l at pH 6.5
Miscible with acetone, cyclohexanone, hexane, methanol, dichloromethane, and
xylene. In propylene glycol 24 g/l at 20 deg C.
In water, 2 ppm at ambient temperature.
Vapor Pressure:
0.055 mPa at 20 deg C
Other Chemical/Physical Properties:
Resistant to decomposition by ultraviolet radiation.
Reasonably stable in acidic and neutral conditions, but rapidly hydrolyzed
in alkaline media (pH 9).
Chemical Safety & Handling:
Hazardous Decomposition:
When heated to decomposition it emits toxic fumes of F- and NOx.
Protective Equipment & Clothing:
Protective clothing, PVC gloves when spraying Fusilade 4E. Also, apron and
full face shield when handling or mixing concentrate. Refer to labels.
Stability/Shelf Life:
Stable for 3 yr at 25 deg C and for 6 months at 37 deg C. Reasonably stable
in acidic and neutral conditions, but rapidly hydrolyzed in alkaline media (pH
9).
Tested stable in storages 40-120 deg F (5-50 deg C).
Disposal Methods:
SRP: At the time of review, criteria for land treatment or burial (sanitary
landfill) disposal practices are subject to significant revision. Prior to implementing
land disposal of waste residue (including waste sludge), consult with environmental
regulatory agencies for guidance on acceptable disposal practices.
Occupational Exposure Standards:
Manufacturing/Use Information:
Major Uses:
The active ingredient is no longer contained in any registered pesticide products
... "cancelled."
Selective post-emergence herbicide.
Highly selective post-emergence grass killer. It will control both annual
and perennial grasses.
Methods of Manufacturing:
n-Butanol + 2-(4-chlorophenoxy)propionic acid + 2-hydroxy-5-(trifluoromethyl)pyridine
(esterification/ether formation)
General Manufacturing Information:
Not registered for use in the U.S.
Formulations/Preparations:
Emulsifiable concentrate, wettable powder.
Laboratory Methods:
Analytic Laboratory Methods:
Product analysis of fluazifop-butyl
by GLC with FID (AOAC Methods, 1990, 984.08; CIPAC Handbook, 1988, 1D, 106).
Residues (fluazifop-butyl, fluazifop,
free and conjugates) determined by HPLC of the free acid. Details available
from Zeneca.
Special References:
Synonyms and Identifiers:
Formulations/Preparations:
Emulsifiable concentrate, wettable powder.
Administrative Information:
Hazardous Substances Databank Number: 6644
Last Revision Date: 20000929
Last Review Date: Reviewed by SRP on 9/18/1997
Update History:
Complete Update on 03/13/2000, 2 fields added/edited/deleted.
Complete Update on 06/03/1998, 43 fields added/edited/deleted.