E X T O X N E T
Extension Toxicology Network
A Pesticide Information Project of Cooperative Extension Offices of
Cornell University, Michigan State University, Oregon State University, and
University of California at Davis. Major support and funding was provided
by the USDA/Extension Service/National Agricultural Pesticide Impact
Assessment Program.
| |
Pesticide
Information
Profile
|
Bromacil
Publication Date: 9/93
|
|
TRADE OR OTHER NAMES
Borea, Bromax 4G, Bromax 4L, Borocil, Rout, Cynogan, Uragan,
Isocil, Hyvar X, Hyvar XL, Urox B, Urox HX, Krovar.
REGULATORY STATUS
Bromacil is classified by the U. S. Environmental Protection Agency
(EPA) as a general use herbicide. Dry formulations containing bromacil
must bear the signal word "Caution" and liquid formulations must bear
the signal word "Warning" (29).
INTRODUCTION
Bromacil is an herbicide used for brush control on non-cropland
areas. It is especially useful against perennial grasses. It is also
used for selective weed control in pineapple and citrus crops. It works
by interfering with photosynthesis, the process by which plants use
sunlight to produce energy. Bromacil is available in granular, liquid,
water soluble liquid, and wettable powder formulations (5, 29).
Bromacil is one of a group of compounds called substituted uracils.
These materials are broad spectrum herbicides used for nonselective weed
and brush control on non-cropland, as well as for selective weed control
on a limited number of crops, such as citrus fruit and pineapple (3).
The herbicide is preferably sprayed or spread dry on the soil surface
just before, or during, a period of active weed growth (19).
TOXICOLOGICAL EFFECTS
ACUTE TOXICITY
Liquid formulations of bromacil are moderately toxic, while dry
formulations are relatively non-toxic (29). Hyvar X-L formulation can
be harmful or fatal if swallowed (5, 6, 29). Industrial and
agricultural workers are exposed to the wettable powders and aqueous
emulsions of bromacil through two primary routes of exposure: inhalation
of dusts and sprays, and skin contact with dusts, emulsions and sprays
(3). The herbicide is irritating to the skin, eyes and respiratory
tract (12).
When as little as 100 mg/kg of the herbicide was fed to dogs, it
caused vomiting, watering of the mouth, muscular weakness, excitability,
diarrhea, and dilation of the pupils of the eyes. Rats that were fed
single doses of bromacil experienced initial weight loss, paleness,
exhaustion, and rapid breathing (15). Within four hours of being given
250 mg/kg of this, or a related material (isocil), sheep became bloated
and walked with stilted gaits (5). Bromacil caused mild dermal
irritation when it was applied to the skin of guinea pigs. Rabbits did
not show clinical signs of poisoning, or toxicity, in response to skin
applications of 5,000 mg/kg of the herbicide (1, 5). When bromacil was
put in the eyes of rabbits, there was irritation in the conjunctiva, the
mucous membrane lining of the eye, but there was no injury to the
cornea, the transparent portion of the eyeball (5).
Because bromacil has a low vapor pressure, it is unlikely to
produce vapors which can be inhaled. No deaths occurred when rats were
exposed to approximately 4.8 milligrams of bromacil per liter of air
(mg/l) for four-hours (1, 15).
Bromacil poses a moderate threat when it is ingested by animals
(18). The amount of bromacil that is lethal to one-half (50%) of the
test animals, when it is given orally, is called its acute oral lethal
dose fifty, or LD50. The oral LD50 for bromacil in rats is 5,200 mg/kg,
and in mice is 3040 mg/kg (5, 12, 15).
CHRONIC TOXICITY
Sheep died after being given 250 mg/kg doses of bromacil on four
successive days. One dog survived a single dose of five grams per
kilogram (gm/kg), but rats died after five days of being given repeated
daily doses of 1,500 mg/kg (5). Autopsy revealed enlarged livers in the
rats (5). In another study, rats were fed 0, 2.5, 12.5 or 62.5
mg/kg/day for 2 years. Female rats at the highest dose level exhibited
decreased weight gain. No other toxic effects were observed and a NOAEL
of 12.5 mg/kg/day was established (32). No evidence of toxicity was
detected in dogs fed up to 31.2 mg/kg/day for 2 years (32). In an 18-
month study in which mice were given dietary doses of 12.5, 62.5 or 250
mg/kg/day, changes in the liver and testes were observed at the 62.5
mg/kg dosage (24, 32). Even though chickens appeared to tolerate one
500 mg/kg dose of bromacil, they did show a decrease in weight gain
(23).
The EPA has established a Lifetime Health Advisory (LHA) level of
90 micrograms per liter (ug/l) for bromacil in drinking water. This
means that EPA believes that water containing bromacil at or below this
level is acceptable for drinking every day over the course of one's
lifetime, and does not pose any health concerns. However, consumption
of bromacil at high levels well above the LHA level over a long period
of time has been shown to cause damage to the testes, liver and thyroid
of laboratory animals (31).
Reproductive Effects
Bromacil did not affect the reproduction and lactation performance
of rats fed 0 or 12.5 mg/kg/day for 3 generations (19, 32). Toxic
effects and developmental abnormalities of the musculoskeletal system
were seen in the embryos or fetuses of female rats which inhaled 38
mg/m3 of bromacil for two hours daily, during the 7th to 14th day of
pregnancy (13).
Teratogenic Effects
There was no evidence of birth defects in the offspring of rats
that were given dietary concentrations of 12.5 mg/kg/day nor in rabbits
that were given 7.5 mg/kg/day on days 8 through 16 of pregnancy (1, 32).
No prenatal or teratogenic effects were observed when pregnant rats were
exposed to aerosols of bromacil (165 mg/m3) on days 7 to 14 of pregnancy
(32). Toxic effects and developmental abnormalities were observed in
the fetuses of pregnant rats repeatedly exposed by inhalation to
bromacil (15).
Mutagenic Effects
Several mutagenic screening tests have not found bromacil to be
mutagenic (3, 32).
Carcinogenic Effects
Although bromacil has not been determined to cause cancer, it is
considered by the EPA to be a possible human carcinogen because there is
some limited or uncertain evidence that bromacil causes cancer in
animals receiving high doses of the chemical over the course of their
lifetimes (31, 32).
Thirty-six male and 36 female weanling rats were fed dietary doses
of 2.5, 12.5 or 62.5 mg/kg/day for 2 years. There was no evidence of
carcinogenicity in rats fed 12.5 mg/kg of bromacil. At the 62.5 mg/kg
dose, there was at slight increase in hyperplasia of the thyroid, and
one individual developed benign liver tumors (1, 32). When mice were
fed dietary doses of 0, 12.5, 62.5 or 250 mg/kg/day for 78 weeks, an
increased incidence of both malignant and benign tumors was observed in
the livers of male mice given 250 mg/kg of bromacil. No effect on liver
tumor incidence was observed in female mice (24, 32).
Organ Toxicity
Enlarged livers were revealed in autopsies on rats that died after
five days of repeated doses of bromacil at 1,500 mg/kg/day (5). Sheep
that died after being given 250 mg/kg/day of bromacil on four successive
days showed the following disease-related findings: inflammation of the
mucous membrane that lines the stomach and intestines, or
'gastroenteritis;' congestion and enlargement of the liver; weakened
appearance of the adrenal glands; bleeding of the heart; swollen and
bleeding lymph nodes (5).
Fate in Humans and Animals
A number of studies show that the substituted uracils, the class of
compounds to which bromacil belongs, are absorbed into the body from the
gut and excreted primarily in the urine (14, 16, 32). Small amounts of
bromacil were detected in the milk of lactating cows that were given
five ppm in their food (5). No bromacil was found in the urine or feces
of these cows (16).
ECOLOGICAL EFFECTS
Effects on Birds
The 8-day oral LD50 for bromacil is over 10,000 ppm in mallards and
quail (3).
Effects on Aquatic Organisms
The median tolerance limit, or the concentration of bromacil that
will kill 50% of the exposed fish after 48 hours of exposure, varies
from 40 ppm to 164 ppm, depending on the type of fish tested (3). The
48-hour LC50 for bromacil in bluegill sunfish is 71 ppm, in rainbow
trout is 56-75 ppm, and in carp is 164 ppm (19). The 96-hour LC50 in
fathead minnows is 182 mg/l (33).
Effects on Other Animals (Nontarget Species)
Tadpoles have a 48-hour median tolerance limit of 230 ppm bromacil
(3). The herbicide is not toxic to either aquatic invertebrates or
honeybees (24, 29).
ENVIRONMENTAL FATE
Breakdown of Chemical in Soil and Groundwater
Bromacil binds, or adsorbs, only lightly to soil particles (Koc =
32 g/ml), is soluble in water, and has a relatively lengthy soil half-
life (60 days). For these reasons, bromacil is expected to move (leach)
quite readily through the soil and it can contaminate groundwater. It
was weakly adsorbed by soils when it was applied at rates of 4 and 1.5
l/hr in tests conducted to study the effects of wetting and drying
cycles on the herbicide. After several cycles of wetting and drying,
the herbicide was completely leached from the original application sites
and was concentrated at the outer edges of the wetted zones. Offsite
leaching is the main route by which bromacil disappears from treated
soils. The amount of leaching is dependent on the soil type and the
amount of rainfall or irrigation water. The potential for bromacil to
leach and contaminate groundwater is greatest in sandy soils. In
regular soils, it can be expected to leach to a depth of 2-3 ft (24).
Bromacil was found in Florida's groundwater at 300 parts per billion
(ppb) (21, 32). Bromacil should not be used near drinking water
reservoirs or in well recharge areas because of its mobility in soil.
Directions and precautions listed on product labels must be followed to
minimize potential bromacil movement into groundwater (24, 29, 30).
The other major mode for the disappearance of bromacil from most
treated soils is microbial degradation. Tests show that at increased
temperatures and long exposures to sunlight, there is very little loss
of the herbicide from dry soil. It does not readily volatilize, or
change into a gas, nor does it photodecompose, or break down in sunlight
(19). Laboratory studies show that 5-30% of bromacil is lost six to
nine weeks after application to the soil, as carbon dioxide, an
odorless, colorless gas (11).
When it is applied to the soil, bromacil destroys most annual
plants in the treated area (10). Field dissipation studies have shown
that phytotoxic residues of bromacil have persisted in both sand and
clay soils for longer than 2 years following a single application of 2.6
lb bromacil/acre (32).
Bromacil is long lasting, or persistent, and its half-life, or the
time that it takes for half of it to break down by natural processes, is
greater than 100 days (17). The herbicide had trace (residual) activity
in soil for seven months after being applied at 7.5 kilogram per hectare
(6). On silt loam soils, bromacil has a half-life of five to six months
and can have toxic effects on susceptible crops for up to one year.
Soils with moderate to high organic matter content may retain residues
for one to two years, but a soil half-life of three to seven months is
more likely. An even shorter half-life is possible in sandy soils
treated with bromacil due to its movement out of the soil and into
groundwater via leaching (23, 24). Eighteen months after 22.4 kg of
bromacil was sprayed on abandoned field sites, residues of the herbicide
were detectable, in decreasing amounts, in loamy sand, silt loam, silty
clay loam and light silty clay loam soils. In all four soil types,
organic matter content, cation-exchange capacity, total nitrogen and
soluble salt concentrations were significantly correlated with residue
persistence (19).
Breakdown of Chemical in Water
There is little information available on the breakdown rate of
bromacil in water, although a two-month half-life is suggested for this
herbicide in clean river water which is low in sediment (24).
Breakdown of Chemical in Vegetation
In plants, bromacil is taken up rapidly by the roots and slightly
absorbed through the leaves (11, 25). When it is applied at 10 ppm,
some types of algae have slowed growth, but most strains are unaffected
(23). Improper application of bromacil will destroy shade trees and
other desirable vegetation. Label instructions should be followed
carefully. Equipment and containers should not be emptied or rinsed out
near desirable trees or shrubs (24). No breakdown products
(metabolites) of bromacil were found in tests done on maize (corn) and
beans (19).
PHYSICAL PROPERTIES AND GUIDELINES
Bromacil is an odorless, white crystalline solid (1, 3). It is
chemically stable under normal storage conditions, but may pose a slight
fire hazard when exposed to heat or flame. It slowly decomposes in the
presence of strong acids and poses a fire and explosion hazard in the
presence of strong oxidizers (15). Technical bromacil and its dry
formulations are non-flammable, but some liquid formulations are
combustible (25). When heated to decomposition, bromacil emits highly
toxic and corrosive fumes of bromides and toxic oxides of nitrogen and
carbon (15, 18). Airborne bromacil dust may ignite (5).
Bromacil formulations are compatible with most herbicides with
which they might be mixed. However, water-soluble formulations are not
compatible with products that greatly reduce the spray of suspensions
(e.g., AMS, amitrole, etc.) and may be precipitated by pesticides
containing soluble calcium salts (19). When used with water-soluble
formulations of bromacil, weed killers that contain soluble calcium
salts can form precipitates (25). This herbicide should be stored in a
cool, dry place (2).
Breathing of bromacil spray mist, as well as eye, skin and clothing
contact with this herbicide, should be avoided. A thorough washing
after handling is advised (2).
Occupational Exposure Limits:
| 1 ppm (10 mg/m3) OSHA TWA (15) |
| 1 ppm (10 mg/m3) ACGIH TWA (15) |
| 2 ppm ACGIH STEL (32) |
| 1 ppm (10 mg/m3) NIOSH |
| Recommended TWA (15) |
Physical Properties:
| CAS#: | 314-40-9 |
| Specific gravity: | 1.55 at 25 degrees C (25) |
| H2O solubility: | 813 - 815 ppm (0.0815%) at 25 degrees C (21, 27, 29) |
| Solubility in other solvents: |
moderately soluble in acetone, strong
aqueous bases, acetonitrile, and ethyl alcohol. Only slightly soluble
in hydrocarbons (29).
- Xylene: 3.2 g/100 ml (3, 25)
- Acetone: 16.7 g/100 ml (3, 25)
- acetonitrile: 7.1 g/100 ml (25)
- strong base: 8.8 g/100 ml (3)
- ethyl alcohol: 13.4 g/100 ml (3)
- sodium hydroxide(3% aqueous): 8.8 g/100 ml (25)
|
| Melting point: | 157.5-160 degrees C (316-320 degrees F) (3, 1, 29) |
| Flash point: | Combustible (29) |
| Decomposition temperature: | |
| Vapor Pressure: | 8 x 10 to the minus 4 power Torr at 100 degrees C (1, 3) |
| Kow: | log Kow = 2.61 (9); 1.33 (8, 26); 2.02 (20) |
| Koc: | 109 (calculated); soil-water distribution coefficient divided by the organic carbon content and calculated by log Koc 3.64 - 0.55 (log water solubility in ppm) +/-1.23 (21); 210 (8, 26); 1.2/2.1 (4); 72 (7); 32 g/ml (30) |
| Kd/mobility: | 0.2-1.8 (soil-water distribution coefficient or adsorption constant from column leaching or TLC studies) (21) |
| Chemical Class/Use: | Substituted uracil herbicide |
| NOEL: | in two-year feeding studies, greater than 250 ppm and less than 1,250 ppm in rats; 1,250 ppm in dogs (1) |
| ADI: | 130 ug/kg/day, based on a 2-year rat feeding study using a NOAEL of 12.5 and a 100-fold uncertainty factor (32). |
BASIC MANUFACTURER
Du Pont Agricultural Products
Walker's Mill, Barley Mill Plaza
PO Box 80038
Wilmington, DE 19880-0038
Review by Basic Manufacturer:
Comments solicited: October, 1992
Comments received: November, 1992
REFERENCES
American Conference of Governmental Industrial Hygienists, Inc.
1986. Documentation of the threshold limit values and biological
exposure indices. Fifth edition. Cincinnati, OH: Publications Office,
ACGIH.
Berg, G. L., ed. 1986. Farm chemicals handbook. Willoughby, OH:
Meister Publishing Company.
Clayton, G. D. and F. E. Clayton, eds. 1981. Patty's industrial
hygiene and toxicology. Third edition. Vol. 2: Toxicology. NY: John
Wiley and Sons.
Farmer, W. J. 1976. Leaching, diffusion, and sorption. In: A
literature survey of benchmark pesticides. Science Communication
Division, George Washington University Medical Center. (U. S. EPA
contract no. 68-01-2889). Washington, DC
Gosselin, R. E., et al. 1984. Clinical toxicology of commercial
products. Fifth edition. Baltimore, MD: Williams and Wilkins.
Hartley, D. and H. Kidd, eds. 1983. The agrochemicals handbook.
Nottingham, England: Royal Society of Chemistry.
Kenaga, E. E. and C. A. I. Goring. 1980. Relationship between
water solubility, soil sorption, octanol-water partitioning and
concentration of chemicals in biota. In J. G. Eaton, P. R. Parrish, and
A. C. Hendricks (eds.). Aquatic Toxicology. ASTFM STP 707, pp. 78.
Philadelphia: Amer. Soc. Testing and Materials.
Leo, A. 1978. Report on the calculation of octanol/water log p
values for structures in the U.S. Environmental Protection Agency files.
Claremont, CA.
Li, Fred. 1982. Technical data submitted in support of the San
Luis drain report of waste discharge. File report. Branch of
Scientific Resources, USBR Department of Interior. (Contract # 2-0-20-
0221). Sacramento, CA.
Melnikov, N. N. 1971. Chemistry of pesticides. NY: Springer-
Verlag, Inc.
Menzie, C. M. 1974. Metabolism of pesticides. U.S. Department
of the Interior. Fish and Wildlife Service Special Scientific Report:
Wildlife. Washington, DC: U. S. Government Printing Office.
Morgan, D. P. 1982 (Jan.). Recognition and management of
pesticide poisonings. Third edition. U. S. Environmental Protection
Agency. Washington, DC: U. S. Government Printing Office.
National Institute for Occupational Safety and Health (NIOSH).
1981-1986. Registry of toxic effects of chemical substances (RTECS).
Cincinnati, OH: NIOSH.
National Research Council, Safe Drinking Water Committee. 1977.
Drinking water and health. Washington, DC: National Academy of
Sciences.
Occupational Health Services, Inc. 1991 (March 28). MSDS for
Bromacil. OHS Inc., Secaucus, NJ.
Paulson, G. D. 1975. Metabolic fates of herbicides in animals.
NY: Springer-Verlag.
Rao, P. S. C., et al. 1983 (Sept.). Pesticides and their
behavior in soil and water. Florida Cooperative Extension Service.
Institute of Food and Agricultural Sciences, University of Florida.
Soil science fact sheet adapted from: Herbicide Injury, Symptoms and
Diagnosis, Skroch and Sheets, eds. 1981 (Dec.). North Carolina
Agricultural Extension Service. AG-85.
Sax, N. I. 1984. Dangerous properties of industrial materials.
Sixth edition. NY: VanNostrand Reinhold Company.
TOXNET. 1975-1986. National library of medicine's toxicology
data network. Hazardous Substances Data Bank (HSDB). Public Health
Service. National Institute of Health, U. S. Department of Health and
Human Services. Bethesda, MD: NLM.
U. S. Environmental Protection Agency. 1984 (Dec.). User's
manual for the pesticide root zone model (PRZM). Release 1. Athens,
GA: Environmental Research Laboratory.
_____. 1984. Memorandum from Stuart Z. Cohen. List of potential
groundwater contaminants. Office of Pesticides and Toxic Substances.
Washington, DC. Photocopy.
_____. 1982 (Sept.). Guidance for the reregistration of
pesticide products containing bromacil as the active ingredient. Office
of Pesticide Programs, Registration Division. Washington, DC.
_____. 1975 (Mar.). Initial scientific and minieconomic review
of bromacil. Office of Pesticide Programs. EPA-540/1-75-006.
Washington, DC.
VanDriesche, R. G. 1985 (Feb.). Pesticide profiles: Bromacil.
Cooperative Extension Service. Department of Entomology, University of
Massachusetts. Amherst, MA: Cooperative Extension Service.
WSSA Herbicide Handbook Committee. Herbicide Handbook of the Weed
Science Society of America, 6th Ed. WSSA, Champaign, IL. 1989.
Woodard, R. 1985. Project report. Interagency delta health
aspects monitoring program. California Department of Water Resources
(Central District).
Worthing, C. R., ed. 1983. The pesticide manual: A world
compendium. Croydon, England: The British Crop Protection Council.
Hayes, W.J. and E.R. Laws (ed.). 1990. Handbook of Pesticide
Toxicology, Vol. 3, Classes of Pesticides. Academic Press, Inc., New
York.
Meister, R.T. (ed.). 1992. Farm Chemicals Handbook '92. Meister
Publishing Company, Willoughby, Ohio.
U. S. Department of Agriculture, Soil Conservation Service. 1990
(Nov.). SCS/ARS/CES Pesticide Properties Database: Version 2.0
(Summary). USDA - Soil Conservation Service, Syracuse, NY.
U. S. Environmental Protection Agency. 1989 (Jan.). Health
Advisory Summary: Bromacil. US EPA, Washington, DC.
_____. 1988 (Aug.). Bromacil: Health Advisory. Office of
Drinking Water, US EPA, Washington, DC.
Du Pont Agricultural Products. 1990 (Oct. 4). Material Safety
Data Sheet for Bromacil Technical. Du Pont, Registration and Regulatory
Affairs, Wilmington, DE.
Disclaimer: Please read
the pesticide label prior to use. The information contained at this web
site is not a substitute for a pesticide label. Trade names used herein
are for convenience only; no endorsement of products is intended, nor is
criticism of unnamed products implied. Most of this information is historical
in nature and may no longer be applicable.
To Top
For more information relative to pesticides and their use in New York State, please contact the PMEP staff at:
| |
5123 Comstock Hall
Cornell University
Ithaca, NY 14853-0901
(607) 255-1866
|
|
 |
This site is supported, in part, by funding from the
 |
Questions regarding the development of this web site should be directed to the
PMEP Webmaster
