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.
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Pesticide
Information
Profile
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Diquat dibromide
Publication Date: 9/93
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TRADE OR OTHER NAMES
Aquacide, Dextrone, Reglone, Reglox, Weedtrine-D, Aquakill,
Vegetrole, Deiquat, Reglon, Tag.
REGULATORY STATUS
Diquat dibromide is classified as a general use herbicide by the
U.S. Environmental Protection Agency (EPA) (7). A registration standard
was issued by EPA in June, 1986. Check with specific state regulations
for local restrictions that may apply to this chemical.
Based on its assessment by EPA as a moderately toxic material,
containers of diquat bear labels with the signal word, "WARNING" (34).
INTRODUCTION
Diquat dibromide is an herbicide and plant growth regulator. It is
a quick-acting contact herbicide, causing injury only to the parts of
the plant to which it is applied (18, 38). It is nonselective, meaning
that it does not spare 'nontarget' plants from its herbicidal effects
(21). Diquat is referred to as a desiccant because it causes a leaf or
an entire plant to dry out quickly. It is not residual, that is, it
does not leave any trace of herbicide on or in plants, soil, or water.
It is used to desiccate potato vines and seed crops, to control
flowering of sugarcane, and for industrial and aquatic weed control (35,
39).
TOXICOLOGICAL EFFECTS
ACUTE TOXICITY
Diquat dibromide is a moderately toxic chemical (34). It may be
fatal to humans if swallowed, inhaled, or absorbed through the skin (4).
Concentrated solutions may cause severe irritation of the mouth, throat,
esophagus and stomach followed by nausea, vomiting, diarrhea, severe
drying out of bodily tissues, gastrointestinal discomfort, chest pain,
diarrhea, kidney failure, and toxic liver damage (24, 36, 42). Very
large doses of the herbicide can result in convulsions and tremors (36).
Rats given lethal doses of diquat showed few signs of illness during the
first 24 hours. They then exhibited lethargy, pupil dilation,
respiratory distress, weight loss weakness and finally death over the
course of 2 to 14 days after dosing. Similar patterns of symptoms
occurred in mice, guinea pigs, rabbits, dogs, cows and hens (38).
Diquat dibromide is acutely toxic when it is absorbed through the
skin and the possibility for poisoning increases with repeated exposure
(35). Dermal adsorption is higher where the skin is cut or abraded
(36). Although absorption is reportedly low following dermal exposure,
the demonstrated toxicity of this compound is sufficient to raise
serious human health concerns. Small amounts of diquat can cause skin
irritation and sores, as well as delayed healing of cuts and wounds
(37). When absorbed through the skin, some commercial concentrate
formulations of diquat can cause symptoms similar to those that occur
when it is eaten. There have been reports of workers who have had
softening and color changes in one or more fingernails after contact
with concentrated diquat dibromide solutions. In some instances, the
nail was shed, and did not grow in again (18). A single dose of diquat
was not irritating to the skin of rabbits. Repeated dermal doses cause
mild redness, thickening, and scabbing (38).
Diquat dibromide also causes eye irritation (5, 27). Several cases
of severe injury to human eyes have been reported after accidental
splashings. In each case, initial irritation was mild, but after
several days, serious burns and sometimes scarring of the cornea
developed (12). Moderate to severe membrane irritation occurred when
diquat was put in the eyes of rabbits (5).
Direct or excessive inhalation of diquat dibromide spray mist or
dust may result in oral or nasal irritation, nosebleeds, headache, sore
throat, coughing, and symptoms similar to those from ingestion of diquat
(5, 18).
The amount of a chemical that is lethal to one-half (50%) of
experimental animals fed the material is referred to as its acute oral
lethal dose fifty, or LD50. The lower the LD50 is for a chemical, the
more toxic it is; the higher the LD50, the less toxic it is. The oral
LD50 for diquat in rats is 120 mg/kg, 233 mg/kg in mice, 188 mg/kg in
rabbits, 187 mg/kg in guinea pigs and dogs. Cows appear to be
particularly sensitive to this herbicide, with an oral LD50 of 30 to 56
mg/kg (1, 42). The acute dermal LD50 for diquat dibromide is 250-400
mg/kg in rabbits (37).
CHRONIC TOXICITY
Cataract formation is the most significant effect of chronic
exposure to diquat that is currently recognized (35). Cataracts, a
clouding of the eyes which interferes with light entering the eye,
occurred in rats and dogs given 2.5 mg/kg and 5 mg/kg of diquat,
respectively (12). The number of cases of cataracts increased in test
animals (cats and dogs) as the amount of diquat was increased in their
diets. This is referred to as a dose-dependent association between
cataracts and diquat ingestion (5, 1). A single, near-fatal dose will
not produce cataracts. Chronic exposure is necessary (38).
The effects of repeated, or prolonged, dermal contact with diquat
dibromide range from inflammation of the skin, to general bodily
('systemic') poisoning, as evidenced by injury to internal organs,
primarily the kidneys. Chronic exposure may damage skin, which allows
more absorption of the herbicide (5). Repeated applications of 42 mg/kg
of diquat killed four out of six rabbits tested (24). While rats fed 50
mg/kg of diquat for two years did not die from testing, their food
intake and growth was decreased (1).
Repeated inhalation exposure of rats to 1.9 mg/m3 caused
inflammatory changes in connective tissues, damage to the kidneys and
heart, abnormal levels of several liver enzymes, low white blood cell
counts, high red blood cell counts, and depressed cholinesterase
activity (42).
Reproductive Effects
Diquat dibromide does not cause reproductive effects (35). It did
not reduce fertility when tested in experimental animals (4). Rats
receiving 25 mg/kg decreased their food intake and showed slowed growth,
but had unchanged reproduction. Fertility was reduced in male mice
given diquat dibromide during different stages of sperm formation (18).
Neither fertility nor reproduction was affected in a three-generation
study in rats given dietary doses of 0, 12.5 or 25 mg/kg/day of diquat
dibromide, although some growth retardation was seen at the 25 mg/kg/day
dose (38).
Teratogenic Effects
EPA does not consider diquat capable of causing teratogenic effects
(35). However, diquat dibromide is thought by other researchers to have
the potential to cause birth defects. It is referred to as an
experimental teratogen based on a study which showed teratogenic effects
in six-day pregnant rats given intravenous injections of diquat. A
lowest published toxic dose, or TDLO, of 7 mg/kg resulted from this
study (27). Growth retardation was seen in test animals given extremely
high doses of diquat. No deformities were found in the unborn offspring
of pregnant rats that were injected intraperitoneally with 0.5 mg/kg of
diquat daily during organogenesis, the stage of fetal development in
which organs are formed (12). Pregnant rats died when they were
injected with 14 mg/kg of diquat dibromide. Upon examination of the
unborn rats, there was evidence of skeletal defects of the collar bone,
as well as little or no ear bone formation (28). While no actual
teratogenesis occurred in rats given single abdominal injections during
the 7th to 14th days of pregnancy, many rats did not have normal weight
gain and bone formation in the unborn was decreased (27).
Mutagenic Effects
EPA has required more testing on the capability of this herbicide
to cause mutations, since available information is contradictory (35).
Diquat dibromide is not known to cause permanent changes in genetic
material and is therefore not considered a mutagen (18). No mutagenic
effects were seen in mice given ten mg/kg of diquat orally for five days
(6).
Carcinogenic Effects
Diquat dibromide is not classified as a tumor-causing chemical (6,
15, 35). An 80-week feeding study showed that dietary doses of 15
mg/kg/day of diquat did not cause tumors in rats (10). Likewise,
dietary levels of 36 mg/kg/day for two years did not induce tumors in
rats (38).
Organ Toxicity
Based on records of suicidal ingestion of diquat by humans as well
as diquat-feeding studies of monkeys, it has been concluded that diquat
is most harmful to the gastrointestinal tract (GIT), kidneys, and liver.
Severe congestion and ulceration of the stomach and bowel are produced
by the herbicide. After large doses of diquat are given, there is
evidence of stretching and irritation of the GIT and thickening of the
walls of the alveoli, or air cells of the lungs (15). When enough
diquat is given, the fat in the liver goes through extreme changes.
Acute death occurs in the cells of the small glandular tubes that
process urine in the kidney. Cataracts are caused when smaller amounts
of diquat are given. While diquat dibromide appears to primarily affect
the tissue lining of the eye lens and the kidneys, water is apparently
removed from other tissues as well. Dehydration can result. The amount
of water which is removed depends on how much diquat dibromide is given
(18). Poisoning by diquat may affect the liver and kidneys (42).
Fate in Humans and Animals
Diquat dibromide may be absorbed by humans following oral
ingestion, dermal exposure or inhalation of spray mists. Studies
indicate that absorption from the gut into the bloodstream is low. Oral
doses of diquat are metabolized mainly within the intestines rather than
in the body proper, with metabolites being excreted in the feces. Only
a small percentage of oral doses are absorbed into the bloodstream and
then excreted in the urine. When rats were fed radio labeled diquat,
only 6% of the dose was recovered in the urine. When exposure occurs
through routes other than oral, diquat enters the bloodstream and is
rapidly eliminated in the urine. Following subcutaneous injection in
rats, excretion of about 90% of the dose occurred in the urine on the
first day and almost all of the remainder on the next day (15, 21, 31,
35, 38). Complete elimination of the herbicide was seen in urine and
feces of rats within four days of administration of oral doses of five
to ten mg/kg of diquat dibromide (17). When diquat was fed to hens, 70-
80% was unchanged when it was excreted in the feces (6). In cattle
0.004 to 0.015% of an oral dose was recovered in the milk and 0.4 to
2.6% of the dose was found in the urine (38).
ECOLOGICAL EFFECTS
Effects on Birds
Diquat dibromide ranges from moderately toxic to practically
nontoxic to birds, depending on the species (35). Its acute oral LD50
in twelve young male mallards was 564 mg/kg. Signs of poisoning in
these birds included instability, wing-drop and lack of movement (19).
The oral LD50 for diquat was 200-400 mg/kg in hens (6).
Effects on Aquatic Organisms
Diquat dibromide is slightly toxic to fish. Its toxicity to fish,
and food organisms on which fish survive, has been reported in many
studies. It appears to be less toxic in hard water (30). The lethal
concentration fifty, or LC50 is that concentration of a chemical in air
or water that kills half of the experimental subjects exposed to it for
a specific time period. The 8-hour LC50 for diquat in rainbow trout is
12.3 ppm, and 28.5 ppm in Chinook salmon (25). The 96-hour LC50 in
northern pike is 16 ppm and 20.4 ppm in fingerling trout (13, 29). The
shell growth of eastern oysters was not noticeably affected with
exposure to 1 ppm of diquat for 96 hours (25).
Some species of fish may be harmed, but not actually killed, by
sublethal levels of diquat dibromide. Oxygen can become depleted in
diquat-treated water by decaying aquatic plants. This decreases the
amount of oxygen available for fish survival. Research indicates that
yellow perch suffer significant respiratory stress when herbicide
concentrations in the water are similar to those normally present during
aquatic vegetation control programs (3). Strip application of the
herbicide over water is recommended to prevent large scale fish kills
(4).
There is little or no bioconcentration of diquat dibromide in fish.
Bioconcentration is the buildup or accumulation of a chemical in plants
and/or animals. One investigation into the persistence of diquat in
fish showed that one half of the herbicide was lost in less than three
weeks (20, 25).
Effects on Other Animals (Nontarget species)
Diquat dibromide is not toxic to honey bees. Cows are particularly
sensitive to the toxic effects of this material (1, 17).
ENVIRONMENTAL FATE
Breakdown of Chemical in Soil and Groundwater
When diquat dibromide comes in contact with soil, it becomes
strongly adsorbed to clay particles or organic matter in the soil for
long periods of time (Koc - 100,000 g/ml). The strong chemical bonds
formed by diquat adsorption to soil particles make the herbicide
biologically and chemically inactive. That is, in certain soils it is
unlikely to be:
- carried away, or leached, by water seeping through the soil;
- taken up by plants;
- broken down by microbes in the soil in a process called microbial degradation; or
- broken down by sunlight (photochemical degradation).
Traces, or residues, of diquat
have been found to persist in soil for many years with very little
degradation (8, 21, 32, 36, 40).
Soil capacity for adsorption of diquat is so high in comparison to
the rates at which it is applied that there is little possibility that
leaching or groundwater contamination will occur. Field and laboratory
tests show that diquat usually remains in the top inch of soil for long
periods of time after it is applied (31, 32). However, there is also
evidence that diquat has the ability to eventually use up, or saturate,
all the available adsorption sites on soil clay particles. Groundwater
quality can be affected if soil adsorption sites become totally
saturated because water moving down through the soil can carry any non
adsorbed herbicide into the groundwater. More research is needed for a
better understanding of the potential effects on groundwater of long-
term, repeated use of diquat.
Studies on the erosion of diquat-treated soils near bodies of water
indicate that diquat stays bonded to soil particles, remaining
biologically inactive in surface waters, such as lakes, rivers and ponds
(32).
Breakdown of Chemical in Water
Since diquat is purposely applied to water to control the growth of
aquatic weeds, its ability to last as an effective residue has been
studied carefully. These studies suggest that diquat is not persistent
in water (14). When diquat is applied to open water, it disappears
rapidly because it binds to suspended particles in the water. These
particles are then taken up by plants. Diquat dibromide's half-life, or
the period of time that it usually takes for half of the amount of the
material to be broken down by natural processes, is less than 48 hours
in water (31). As affected plants decompose, the adsorbed diquat
rapidly disappears from open waters. Disappearance may be due to
degradation by microbes or sunlight, or due to adsorption to bottom
sediments. Twenty-two days after a weed infested artificial lake was
treated, only 1% of the applied diquat remained in the water and 19% was
adsorbed to sediments. Adsorbed diquat was subject to microbial
degradation (41). Diquat has been found in the bottom soil of pools and
ponds four years after application (12). Diquat will photodegrade in
surface layers of water in 1 to 3 or more weeks when it is not adsorbed
to suspended particles (32, 41).
The EPA requires a 14-day interval between treatment of water with
diquat dibromide and use of treated waters for domestic, livestock, or
irrigation purposes. Swimming, fishing and watering of domestic animals
should not be allowed for at least 14 days after application of the
herbicide to water. The herbicide cannot be used for any purpose in
commercial fish processing areas (35).
Breakdown of Chemical in Vegetation
Diquat is rapidly absorbed by the leaves of plants. Usually, plant
tissues are killed too quickly to allow translocation to other parts of
the plant. The herbicide interferes with cell respiration, the process
by which plants take in oxygen. The chemical structure of diquat is not
changed or degraded within plants. Rather, after it is sprayed on
plants or dead/decaying vegetation, diquat is broken down on the surface
by photochemical degradation (17). The resulting intermediate residues
of diquat are incorporated with the plant materials into the soil,
where, through a process called 'microbial degradation, they are changed
into carbon dioxide by soil microorganisms (21, 32, 36). Diquat
dibromide is also rapidly absorbed by weeds in water, which causes the
concentrations of the material in plant tissue to be higher than in
surrounding water. Low concentrations of the herbicide in water are
adequate for controlling aquatic weeds (31).
Since diquat dibromide is a nonselective herbicide with non-crop
use patterns that overlap endangered plant habitats, it may present a
danger to nontarget plants, including endangered species (35).
PHYSICAL PROPERTIES AND GUIDELINES
Technical diquat, which is greater than 95% pure, forms white to
yellow crystals (38). It is usually marketed in an aqueous solution
which is dark reddish-brown (22, 36).
Diquat is highly soluble in water. It usually decomposes in
alkaline solutions but is stable in neutral or acidic solutions (2).
Diquat degrades when it is exposed to the ultraviolet rays of sunlight
(17).
Diquat contains small amounts of a highly toxic chemical impurity,
ethylene dibromide (EDB). The National Institute for Occupational
Safety and Health (NIOSH) has recommended an occupational exposure limit
for EDB of 0.13 ppm during any 15-minute sampling period (5). When
heated to decomposition, very toxic fumes are emitted from diquat (27).
Diquat is a nonvolatile chemical. This means that it will not vaporize
and become a gas (24).
Diquat is stable under normal temperatures and pressures, but it
may pose a slight fire hazard if exposed to heat or flame. It poses a
fire and explosion hazard in the presence of strong oxidizers. Thermal
decomposition of diquat will release toxic oxides of nitrogen and carbon
and toxic and corrosive fumes of bromides (42).
Diquat is corrosive. Commercial use formulations of diquat contain
corrosion inhibitors, ingredients that slow down or prevent corrosion.
In spite of corrosion inhibitors, concentrated formulations will corrode
metals, especially aluminum, and should be stored only in the original
container. It should not be put into food or drink containers (31).
While it can be mixed with most herbicides, diquat dibromide is
incompatible with anionic wetting agents such as alkyl sulfamates (17).
To reduce skin exposure to diquat dibromide, protective clothing
should be worn when handling the concentrated product, and splashes
should be immediately washed away from eyes and skin. Skin and eye
contact with diquat, especially from drift, should be avoided (17).
Breathing diquat spray (mist) should also be avoided (2). Respiratory
equipment is recommended, especially in situations in which exposure to
drifting spray is possible.
A 24-hour reentry interval is set by EPA for crop sites, golf
courses, and rights-of-way that are treated with diquat dibromide. A
14-day period is also required by EPA between diquat treatment of water
bodies and use of treated water for domestic, swimming, irrigation,
and/or livestock feeding purposes (35). Diquat dibromide may not be
used where commercial fish processing is practiced (9, 32).
Occupational Exposure Limits:
| 0.5 mg/m3 OSHA TWA |
| 0.5 mg/m3 ACGIH TWA |
| 0.5 mg/m3 NIOSH recommended TWA (42) |
Physical Properties:
| CAS #: | 85-00-7 |
| Specific gravity: | 1.22 to 1.27 (36) |
| H2O solubility: | very soluble, 70 gm/100 ml in 20 degrees C water (38) |
| Solubility in other solvents: | insoluble in non-polar organic solvents such as chloroform, diethyl ether, and petroleum ether (1); slightly soluble in alcohol and hydroxylic solvents (35) |
| Melting point: | 335 - 340 degrees C (22) |
| Decomposition point: | decomposes above 300 degrees C (38) |
| Vapor pressure: | negligible, less than 10-5 mbar at 20 degrees C; does not volatilize very much from water or soil (17) |
| Koc: | 100,000 g/ml (42) |
| Kow: | Log octanol/water coefficient = -3.05 (31) |
| Chemical Class/Use: | heterocyclic cationic herbicides -- bipyridilium quaternary ammonium salts |
| NOEL: | for cataract formation in rats: 0.22 mg/kg/day; in dogs: 1.7 mg/kg/day (35) |
| ADI: | 0.005 mg/kg, based on a NOEL of 0.5 mg/kg and a safety factor of 100 (11) |
| PEL: | Health Advisory for drinking water (EPA): tolerances have been established in potable water (0.01 ppm) (2) |
| STEL: | 1.0 mg/m3 (31) |
BASIC MANUFACTURER
Zeneca Ag Products
Wilmington, DE 19897
Review by Basic Manufacturer:
Comments solicited: November, 1992.
Comments received:
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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.
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