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
|
Paraquat
Publication Date: 9/93
|
|
TRADE OR OTHER NAMES
Product names include Crisquat, Dextrone, Dexuron, Gramoxone Extra,
Herba-xone, Ortho Weed and Spot Killer, and Sweep.
INTRODUCTION
Paraquat is a quartenary nitrogen herbicide widely used for broadleaf
weed control. It is a quick acting, non-selective compound, that destroys
green plant tissue on contact and by translocation within the plant. It has
been employed for killing marijuana in the U.S. and in Mexico. It is also
used as a crop desiccant and defoliant, and as an aquatic herbicide (11).
Paraquat is a Restricted Use Pesticide (RUP) and is banned for use in
several Scandinavian countries. Restricted Use Pesticides may be purchased
and used only by certified applicators.
TOXICOLOGICAL EFFECTS
ACUTE TOXICITY
Paraquat is highly toxic to animals by all routes of exposure, and is
labeled with a DANGER-POISON signal word. A single large dose, administered
orally or by injection to animals, can cause excitability and lung congestion,
which in some cases leads to convulsions, incoordination, and death by
respiratory failure.
Paraquat is exceedingly toxic to humans. Many cases of illness and/or
death have been reported (12). The lethal ingestion dose of paraquat in
humans is 35 mg/kg (6). A maximum of 3.5 mg/hour could be absorbed through
the dermal or respiratory route without damage (10).
If swallowed, burning of the mouth and throat often occurs, followed by
gastrointestinal tract irritation, resulting in abdominal pain, loss of
appetite, nausea, vomiting, and diarrhea. Other symptoms of toxicity include
thirst, shortness of breath, and rapid heart rate. Other toxic effects
include kidney failure, lung sores, and liver injury. Some symptoms may not
occur until days after exposure.
Persons with lung problems may be at increased risk from exposure.
Evidence also suggests that long-term, heavy smoking of marijuana contaminated
with paraquat may cause lung scarring (10). Although nose bleeds and lung
irritation may occur if paraquat is inhaled, the risk of serious damage due to
occupational exposure to paraquat is low because of its low vapor pressure.
Direct contact with paraquat solutions or aerosol mists may cause skin
burns, dermatitis, and damage to fingernails. Paraquat splashed in the eye
can irritate, burn, and cause corneal damage and scarring of the eyes.
The oral LD50 of paraquat, in its various forms, for rats ranges from
about 20 mg/kg (10) to 150 mg/kg (6). The oral LD50 of the dichloride form of
paraquat is 196 mg/kg in mice, 50 mg/kg in monkeys, and 48 mg/kg in cats (6).
The oral LD50 of paraquat in the cow is 50-75 mg/kg (6). The dermal LD50 in
rabbits is 236-325 mg/kg.
CHRONIC TOXICITY
No long-term studies on paraquat's effects on humans were found. Several
chronic effects for humans have been inferred from animal studies including
Parkinson's disease and irreversible lung damage (13).
In animal studies, rats showed no effects after being exposed for two
years to paraquat (6). Dogs, however, developed lung problems after being
exposed to high doses for two years (6, 9).
Reproductive Effects
Overall, there is little evidence that paraquat causes adverse effects on
reproduction.
In a long-term rat study, no adverse reproductive effects were reported
(8). Paraquat, administered both orally and by injection to pregnant mice,
did not transfer to the mouse embryos in appreciable quantities. Hens given
high levels of paraquat in their drinking water for 14 days produced an
increased percentage of abnormal eggs (6).
In one suicide, a seven-month pregnant woman swallowed about 2 ounces of
paraquat. The fetal heartbeat disappeared on the 13th day. The mother died
on the 17th day after poisoning. No symptoms of paraquat poisoning were noted
in the body of the fetus (6).
Teratogenic Effects
The weight of evidence suggests that paraquat does not cause birth
defects at doses which might reasonably be encountered. Offspring of mice
dosed with high doses of paraquat during the sensitive period of pregnancy had
less complete bone development than the mice given lower doses. Offspring of
rats given similar treatment showed no developmental defects at any dose, but
fetal and maternal body weights were lower than normal (8). Other studies of
paraquat using rabbits and mice have shown no teratogenic effects (6, 9).
Mutagenic Effects
Paraquat has been shown to be mutagenic in human, microorganism, and
mouse cell assays (8). Paraquat dichloride did not cause mutations in the
sperm of fertile male mice, but pregnancy rates were reduced (6).
Carcinogenic Effects
Mice fed paraquat dichloride for 99 weeks at high levels did not show
cancerous growths. Rats fed high doses for 113 (male) or 124 weeks (female)
developed lung, thyroid, skin, and adrenal tumors (8). Paraquat's
carcinogenic potential has not yet been thoroughly evaluated; however, the EPA
has classified the pesticide as a possible human carcinogen (14).
Organ Toxicity
Paraquat is extremely toxic to mammalian lungs, where it can cause sores,
bleeding, and disease. The lung tissue accumulates paraquat at much higher
rates that do the other organs and tissues in the body (11). However, it can
also damage the heart, liver, kidneys, cornea of the eyes, adrenal glands,
skin, fingernails, and digestive system. Inhalation of paraquat can cause
nasal mucous irritation and bleeding of the gastrointestinal tract (9, 10).
In a study of 30 workers spraying paraquat over a 12-week period,
approximately one-half had minor irritation of the eyes and nose (6). Of 296
spray operators with gross and prolonged skin exposure, 55 had damaged
fingernails as indicated by discoloration, nail deformities, or loss of nails
(6).
Fate in Humans and Animals
Paraquat is not readily absorbed from the stomach, and is even more
slowly absorbed across the skin. This chemical rapidly disappears from the
blood.
In the stomach, the metabolites formed from paraquat breakdown are more
readily absorbed than is paraquat (9) but their toxicity is unknown.
As paraquat concentrates in lung tissue, it is changed to highly reactive
and potentially toxic forms.
Oral doses of paraquat in rats are excreted mainly in the feces, while
paraquat injected into the abdomen leaves through urine (9).
In one study, farm animals excreted over 90% of the administered paraquat
within a few days. It was slightly absorbed and metabolized in the
gastrointestinal tract. Milk and eggs contained small amounts of two paraquat
metabolites (9).
ECOLOGICAL EFFECTS
Paraquat is moderately to highly toxic to many species of aquatic life
including rainbow trout, bluegill, and channel catfish (6).
At high levels, paraquat inhibits the photosynthesis of some algae in
stream waters (5).
Paraquat is rapidly excreted by animals, so tissue accumulation is
unlikely. In rainbow trout exposed for seven days to paraquat, the chemical
was detected in the gut and liver, but not in the meat of the fish.
Aquatic weeds may be a source of bioaccumulation. In one study, four
days after paraquat was applied as an aquatic herbicide, weeds sampled showed
significant residue levels.
Paraquat is non-toxic to honey bees (14).
ENVIRONMENTAL FATE
Ultraviolet light, sunlight, and soil microorganisms can degrade paraquat
to products which are less toxic than the parent compound.
High concentrations of paraquat in marijuana fields have been reported.
Paraquat dichloride droplets decompose when exposed to light after being
applied to maize, tomato, and broad-bean plants. Small amounts of residues
were found in potatoes treated with paraquat as a desiccant, and boiling the
potatoes did not reduce the residue (6).
Paraquat is quickly and strongly adsorbed by soil particles, especially
in clay soil (3). Such bound residues are not available to plants,
earthworms, and microorganisms. Because of its unavailability, and its
resistance to microbial degradation and breakdown by sunlight, paraquat is
long-lived. The bound residues persist indefinitely and are transported in
runoff with the sediment. The reported half-life for paraquat in soil ranges
from 16 months (aerobic laboratory conditions) to 13 years (field study) (7).
Paraquat is not mobile in silt loam and silty clay loams, and is slightly
mobile in sandy loams (8). Paraquat not associated with soil particles can be
decomposed to an non-toxic end product by soil bacteria (10).
Paraquat residues disappear rapidly from water by binding onto aquatic
weeds and by strong adherence to the bottom mud. It has a half-life in
laboratory stream water of 13.1 hours (5). In another study, paraquat
dichloride was stable for up to 30 days. In a third study using low levels in
water, paraquat had a half-life of 23 weeks (8).
Because paraquat quickly adsorbs to soil particles, it resists
decomposition by sunlight. Paraquat sprayed on the surface of a sandy soil
did not degrade when the soil was irradiated with natural sunlight for two
years (8).
Of 721 groundwater samples, only one sample contained paraquat, at a
concentration of 20 ppm (8).
COMMENTS AND PROBLEMS
Paraquat is similar to 1-methyl-4- phenyl-1,2,3-tetrahydropyridine, a
compound which induces a Parkinsonian-like state in humans. In a Canadian
study, the correlation between Parkinson's disease incidence and level of
pesticide use was very strong.
PHYSICAL PROPERTIES AND GUIDELINES
Paraquat salts are colorless, white, or pale yellow crystalline solids,
which are hygroscopic and odorless. The dichloride salt is stable except
under alkaline conditions. The formulated technical grade product is a dark
red solution with an ammonia-like odor. It is corrosive to metals, will react
with strong oxidizers, and tends to be light-sensitive. Paraquat is stable to
heat when in acid or neutral solutions, but is hydrolyzed by alkali solutions.
Paraquat decomposes at high temperatures to form toxic gases and vapors such
as hydrogen chloride, nitrogen oxides, sulfur oxides, and carbon monoxide. Its
molecular weight is 257.18 (8).
The chemical name for paraquat is 1'-Dimethyl-4,4'-bipyridinium. Paraquat
is often formulated as a dichloride salt or a dimethyl sulfate salt. This
chemical is also known as N,N'-dimethyl-4,4'-bipyridinium; N,N'-dimethyl-4,
4'-bipyridinium dication, and o-paraquat dichloride. Under normal storage
conditions, paraquat's shelf-life is indefinite (10).
Exposure Guidelines:
| ADI: | .002 mg/kg (paraquat dichloride); or 0.0045 mg/kg/day (8) (paraquat ion) |
| TLV: | air. |
| TWA: | 0.1 mg/m3 [dichloride and bis(methosulfate)salts] |
Drinking water health advisory: | Drinking Water Equivalent Level (DWEL): 160 ug/L (8) |
Physical Properties:
| CAS #: | 1910-42-5 |
| Solubility in water: | very soluble (20 degrees C) (2) |
| Solubility in solvents: | Paraquat has little to no solubility in organic solvents. The dichloride salt is sparingly soluble in lower alcohols and is insoluble in hydrocarbons. |
| Boiling point: | 175-180 degrees C (decomposes) (2) |
| Vapor pressure: | <10-7 torr(10) Not volatile (2) |
| Log P: | Less than 7.0 |
| Kow: | 2.44 (calculated) (8) |
| Koc: | 15,473-51,856 (1, 4) |
| BCF: | 0.3 (calculated) (6) |
BASIC MANUFACTURER
Zeneca Ag Products
Wilmington, Deleware 19897
Telephone 800-759-4500
Review by Basic Manufacturer:
Comments solicited: November, 1992
Comments received:
REFERENCES
Farmer, W.J. 1976. "Leaching, Diffusion, and Sorption." From A
Literature Survey of Benchmark Pesticides. Science Communication Division of
George Washington University Medical Center.
Hahn, Jr., R.W. and P.A. Jensen. 1974. Water Quality Characteristics
of Hazardous Materials. Vol. 1. Texas A&M University.
Juo, A.S.R. and O.O. Oginni. 1978. Adsorption and desorption of
paraquat in acid tropical soils. J. Environ. Qual. 7 (1): 9-12.
Kenaga, E. 1980. Ecotoxicol. Environ. Safety. 4: 26.
Kosinski, J.R., and M.G. Merkle. 1984. J. Environ. Qual. 13(1):75-
82.
National Library of Medicine. Hazardous Substances Databank.
Paraquat. 1992.
Rao, P.S.C. and J.M. Davidson. 1980. "Estimation of Pesticide
Retention and Transformation Parameters Required in Nonpoint Source Pollution
Models." In Environmental Impact of Nonpoint Source Pollution. M.R. Overcash
and J.M. Davidson, eds. Ann Arbor Science.
U.S. Environmental Protection Agency. Office of Drinking Water.
Paraquat Health Advisory. August 1987. Draft.
Vettorazzi, G. 1979. International Regulatory Aspects for Pesticide
Chemicals. Volume I. CRC Press.
Wagner, S.L. 1983. Clinical Toxicology of Agricultural Chemicals.
Noyes Data Corporation.
Ecobichon, Donald J. 1991. Toxic Effects of Pesticides in Casarett
and Doull's Toxicology. The Basic Science of Poisons. Fourth Edition. Mary
O. Madur, John Doull, and Curtis D. Klaassen editors Pergamon Press, NY.
Stevens, James T. and Darrell D. Summer. 1991. Herbicides in
Handbook of Pesticide Toxicology.Volume 3. Classes of Pesticides. Wayland J.
Hayes and Edward R. Laws editors. Academic Press, NY.
Briggs, Shirley A. 1992. Basic Guide to Pesticides: Their
Characteristics and Hazards. Hemisphere Publishing Corporation.
Philadelphia, PA.
Walker, Mary M. and Lawrence H. Keith. 1992. EPA's Pesticide Fact
Sheet Database. Lewis Publishers. Chelsea, MI.
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